Neoplasma[JOURNAL]
Sun
200 papers
Value of PD-1 and CD28 expression on T lymphocytes in predicting radiation-induced lung injury: a prospective observational study.
Dong L, Li C, Yu J … +2 more , Wang W, Wang Z
Neoplasma · 2026 Jun · PMID 42394417 · Publisher ↗
Radiation-induced lung injury (RILI) remains a major dose-limiting toxicity in thoracic radiotherapy, with risk prediction relying primarily on dosimetric parameters, which show significant individual heterogeneity. This...
Radiation-induced lung injury (RILI) remains a major dose-limiting toxicity in thoracic radiotherapy, with risk prediction relying primarily on dosimetric parameters, which show significant individual heterogeneity. This study aimed to evaluate dynamic changes in peripheral blood T-cell immune checkpoints as predictive biomarkers for ≥ Grade 2 RILI. In this prospective observational study, 274 lung cancer patients receiving thoracic radiotherapy were enrolled. Peripheral blood T-cell subsets (PD-1/CD28 expression on CD4+ and CD8+ cells) were analyzed by flow cytometry before radiotherapy (W0) and at week 2 (W2). The primary endpoint was ≥ Grade 2 RILI, assessed using CTCAE v4.0. With a median follow-up of 19 months, 87 patients (31.8%) developed ≥ Grade 2 RILI. Multivariate Cox analysis identified immunotherapy (HR=1.61, p=0.044), high mean lung dose (HR=2.33, p=0.002), and elevated levels of CD8+PD-1+ (W2, HR=2.18, p=0.030) and CD8+CD28+ (W2, HR=1.73, p=0.025) T cells as independent risk factors. Dynamic monitoring of CD8+PD-1+ and CD8+CD28+ T cells early during radiotherapy provides a novel and independent biological indicator for predicting RILI risk, complementing traditional dosimetric assessment.
The interplay between cancer and follicular fluid: molecular changes and tumor-promoting properties.
Melegová D, Šramková M, Kozics K
Neoplasma · 2026 Jun · PMID 42302181 · Publisher ↗
Follicular fluid is a complex biological microenvironment essential for oocyte maturation and folliculogenesis. Alterations in follicular fluid composition have been associated with reproductive disorders reflecting comp...
Follicular fluid is a complex biological microenvironment essential for oocyte maturation and folliculogenesis. Alterations in follicular fluid composition have been associated with reproductive disorders reflecting compromised oocyte quality. Emerging evidence suggests that malignancies also significantly alter the composition of follicular fluid, potentially compromising the follicular microenvironment and impacting fertility preservation outcomes. Interestingly, the follicular fluid itself exhibits tumor-initiating and tumor-promoting properties, inducing DNA damage, pro-inflammatory signaling, mild proliferation, and suppressing apoptosis. Understanding cancer-associated follicular fluid alterations may improve fertility care, identify early biomarkers, and inform strategies for ovarian cancer prevention and therapy. This review aims to summarize current knowledge on how cancer can alter follicular fluid composition and its role in ovarian malignancies.
The miR-5681b/Beclin-1 axis regulates tumor autophagy to affect the proliferation and apoptosis of prostate cancer cells.
Zhang Y, Li J, Li Q … +1 more , Cao Y
Neoplasma · 2026 Jun · PMID 42222931 · Publisher ↗
Prostate cancer (PCa) is a leading cause of cancer-related mortality among men. This study aims to investigate the regulatory effect of microRNA (miR)-5681b, a potential upstream miR of Beclin-1, on PCa cell proliferatio...
Prostate cancer (PCa) is a leading cause of cancer-related mortality among men. This study aims to investigate the regulatory effect of microRNA (miR)-5681b, a potential upstream miR of Beclin-1, on PCa cell proliferation and apoptosis. Two PCa cell lines (PC3 and LNCaP cells) with relatively low miR-5681b expression were treated with miR-5681b mimic, pcDNA3.1-Beclin-1, or an autophagy activator rapamycin. A xenograft tumor model was established in nude mice, and the tumor-bearing mice were treated with agomir miR-5681b. The levels of miR-5681b, Beclin-1 mRNA, and apoptosis- and autophagy-associated proteins were evaluated using western blot and RT-qPCR. The binding between Beclin-1 and miR-5681b was testified by dual-luciferase reporter gene assay. Cell biological behaviors, as well as Ki-67-positive cells and apoptosis in mouse tumor tissues, were examined. The results showed that miR-5681b was downregulated in PCa cells and targeted Beclin-1. miR-5681b overexpression in PCa cells significantly suppressed cell proliferation and B-cell lymphoma 2 (Bcl-2) levels while augmenting cell apoptosis and the levels of Bcl-2-associated X (Bax) and cleaved caspase-3. Importantly, miR-5681b inhibited PCa cell proliferation and autophagy but promoted PCa cell apoptosis, whereas Beclin-1 upregulation reversed these effects. Activating autophagy also reversed miR-5681b-regulated proliferation and apoptosis of PCa cells. In vivo, miR-5681b overexpression inhibited PCa tumor growth by modulating the Beclin-1-mediated autophagy pathway. Collectively, these findings suggested that miR-5681b was lowly expressed in PCa cells, and miR-5681b overexpression inhibited autophagy by targeting Beclin-1, thereby suppressing the growth of PCa.
IL-17 promotes H1299 cell proliferation via LINC01518/miR-20a-5p/E2F1 axis in non-small cell lung cancer.
Zhao C, Ruan Y, Liao J … +7 more , Ying S, Wu N, Ma P, Wu J, Wang Y, Shu Y, Qiu W
Neoplasma · 2026 Jun · PMID 42207612 · Publisher ↗
Human non-small cell lung cancer (NSCLC) is an inflammation-related disease. Although IL-17-induced NSCLC cell proliferation that can be regulated by transcription factors has been demonstrated, the role and mechanism of...
Human non-small cell lung cancer (NSCLC) is an inflammation-related disease. Although IL-17-induced NSCLC cell proliferation that can be regulated by transcription factors has been demonstrated, the role and mechanism of other regulatory molecules, such as long noncoding RNAs (lncRNAs), in cell proliferation remains unclear. In this study, we screened and verified the expression of aberrant lncRNAs in NSCLC cell lines (H1299 and PC9) stimulated with IL-17, and found that LINC01518 was not only overexpressed, but also enhanced cell proliferation through IL-17/IL-17RA. Further mechanism investigation discovered that IL-17-upregulated LINC01518 was mainly localized in the cytoplasm, and it could combine with miR-20a-5p through a "sponge" function, decreasing miR-20a-5p induction, while LINC01518 and miR-20a-5p co-overexpression could partially reverse the cell proliferation mediated by LINC01518 alone. LINC01518 increase or miR-20a-5p decrease could elevate E2F1 level boosting H1299 cell proliferation exposed to IL-17, while miR-20a-5p and E2F1 co-overexpression partially restored the cell proliferation inhibition from miR-20a-5p upregulation. Besides, the xenograft tumor experiments of mice confirmed that LINC01518 overexpression indeed promoted tumor growth, cell proliferation, miR-20a-5p downregulation, and E2F1 upregulation. While LINC01518 knockdown reduced tumor growth, cell proliferation, miR-20a-5p downregulation, and E2F1 upregulation induced by IL-17 stimulation. Taken together, these findings reveal that the LINC01518/miR-20a-5p/E2F1 axis contributes to IL-17-induced cell proliferation in NSCLC.
BATF2 reverses multidrug resistance of gastric cancer cells and centrosome clustering by suppressing ATM phosphorylation.
Yang W, Song J, Jiang L … +6 more , Zhu W, Wang J, Huang Q, Hu J, Zeng R, Wu B
Neoplasma · 2026 Jun · PMID 42059142 · Publisher ↗
Chromosome instability (CIN) is a major contributor to drug resistance and recurrence. As a crucial mechanism of CIN, centrosome clustering has emerged as a promising therapeutic strategy. However, the roles and regulato...
Chromosome instability (CIN) is a major contributor to drug resistance and recurrence. As a crucial mechanism of CIN, centrosome clustering has emerged as a promising therapeutic strategy. However, the roles and regulatory mechanisms of centrosome clustering in gastric cancer (GC) remain unclear. BATF2 was previously identified as a key modulator of multidrug resistance (MDR) in GC. To examine the involvement of centrosome clustering in the mechanism by which BATF2 reverses MDR in GC, adriamycin (ADR)- and vincristine (VCR)-resistant cell lines, NCI-N87/ADR and NCI-N87/VCR, were used for investigations. Expression of BATF2 was downregulated in both drug-resistant cells, particularly in NCI-N87/ADR cells. Cells with BATF2 knockdown exhibited higher cell viability and lower apoptosis rates, and such changes were reversed by BATF2 overexpression. The enhanced centrosome clustering in cells transfected with sh-BATF2 was accompanied by increased KIFC1 expression, which was inhibited after BATF2 overexpression. BATF2 reversed MDR and inhibited centrosome clustering by inhibiting ATM phosphorylation, which was evidenced by ATM overexpression. Meanwhile, KU-60019, a specific inhibitor of ATM, could markedly reverse the pro-tumor effects of BATF2 knockdown. In conclusion, BATF2 is a potential target for reversing MDR in GC, and targeting KIFC1-related centrosome clustering by suppressing ATM phosphorylation is proposed as a key mechanism.
circRNA circ-ZEB1 promotes gallbladder carcinomas progression by regulating the miR-144-3p/ZEB2 axis.
Huang L, Zhang Y, Yang F … +2 more , Ling Y, Zhou X
Neoplasma · 2026 Apr · PMID 42054277 · Publisher ↗
Gallbladder cancer (GBC) is the most common and aggressive type of tumor occurring in the biliary system. Several studies have indicated the possible functions of circular RNAs (circRNAs) in GBC tumorigenesis. This resea...
Gallbladder cancer (GBC) is the most common and aggressive type of tumor occurring in the biliary system. Several studies have indicated the possible functions of circular RNAs (circRNAs) in GBC tumorigenesis. This research aimed to explore the roles of a novel circRNA, circ-ZEB1 (hsa_circ_0093509), in GBC. The expressions of circ-ZEB1, miR-144-3p, and ZEB2 in GBC cells were detected using RT-qPCR or western blot. The subcellular localization of circ-ZEB1 in GBC cells was determined. The function of circ-ZEB1, miR-144-3p, and ZEB2 in GBC cells was assessed by using CCK-8, EdU staining, colony formation, or Transwell assays. The relationship among miR-144-3p and corresponding targets, circ-ZEB1 and ZEB2, was confirmed. Additionally, xenograft experiments were conducted to assess the role of circ-ZEB1 in tumor growth in vivo. circ-ZEB1 was predominantly found in the cytoplasmic region of GBC cells and was upregulated in the GBC cell lines. Suppression of circ-ZEB1 reduced the proliferation and migration of GBC-SD and SGC-996 cells. Knockdown of circ-ZEB1 attenuates tumor growth in vivo. Mechanistically, circ-ZEB1 sponged miR-144-3p, which targeted ZEB2. Additionally, inhibition of miR-144-3p rescues the effects of circ-ZEB1 or ZEB2 knockdown. These results clarified a vital role of the circ-ZEB1/miR-144-3p/ZEB2 axis in GBC advancement, and may serve as a novel therapeutic target for GBC treatment.
YBX1 promotes the stemness and metastasis of NSCLC cells by promoting CDCA8 expression.
Wu X, Hu Y, Ji X … +1 more , Zhao Y
Neoplasma · 2026 Apr · PMID 42054276 · Publisher ↗
Cancer stemness is a major therapeutic challenge in oncology. This study investigated the functional role and molecular mechanism of cell division cycle-associated 8 (CDCA8) in non-small cell lung cancer (NSCLC) stem cel...
Cancer stemness is a major therapeutic challenge in oncology. This study investigated the functional role and molecular mechanism of cell division cycle-associated 8 (CDCA8) in non-small cell lung cancer (NSCLC) stem cells. In this study, NSCLC and paracancerous tissues were collected. The lung adenocarcinoma cell line A549 and the lung squamous cell carcinoma cell line NCI-H520 were used. The stem-like cell population in A549 and NCI-H520 was isolated by CD44+ fluorescence-activated cell sorting. Gene expression was detected by quantitative real-time PCR, western blotting, and immunohistochemical staining. Cell stemness was assessed by biomarker (SOX and NANOG) expression detection, colony formation assay, and sphere-formation assay. Cell migration and invasion ability were determined by the Transwell experiment. Our results showed that CDCA8 expression was higher in NSCLC tissues than in paracancerous tissues. CDCA8 overexpression enhanced stemness properties, as evidenced by increased biomarker expression and colony formation, larger sphere size, and enhanced migratory/invasive capacity. Conversely, CDCA8 knockdown had the opposite effect. Mechanistically, we identified Y-box binding protein 1 (YBX1) as a direct binding protein of CDCA8 mRNA that positively regulated CDCA8 expression. YBX1 overexpression had a similar effect to CDCA8. Furthermore, recovery experiments revealed that the stemness-promoting effect of YBX1 was reversed by CDCA8 knockdown. These findings were further validated in xenograft models, confirming that the YBX1/CDCA8 axis promoted tumorigenesis in vivo. Collectively, our study reveals that YBX1 enhances cell stemness and metastasis of NSCLC by promoting CDCA8 expression. Our findings established a new mechanism that maintains NSCLC stemness and may provide novel biomarkers.
Expression and prognostic significance of CD66b in diffuse large B-cell lymphoma.
Tao Y, Wu Y, Zhang X … +2 more , He S, Miao X
Neoplasma · 2026 Apr · PMID 42054275 · Publisher ↗
Diffuse large B-cell lymphoma (DLBCL) is the most common type of non-Hodgkin lymphoma in the world. It exhibits high heterogeneity and invasiveness and is prone to developing treatment resistance. Therefore, there is an...
Diffuse large B-cell lymphoma (DLBCL) is the most common type of non-Hodgkin lymphoma in the world. It exhibits high heterogeneity and invasiveness and is prone to developing treatment resistance. Therefore, there is an urgent need for good prognostic evaluation indicators and therapeutic targets. In recent years, immunotherapy has become a research hotspot for DLBCL. Tumor-associated neutrophil (TAN) is widely expressed in various tumors and is an important component of the immune microenvironment. However, there have been few studies on the role of TAN in DLBCL. This study has demonstrated that CD66b, which is a marker of TAN, is a good prognostic marker of DLBCL and its expression is related to the prognosis of DLBCL patients. The expression level of CD66b is also closely correlated with the objective response rate of the R-CHOP treatment regimen in DLBCL patients with non-GCB subtype. The expression level of CD66b has a high reference value for the determination of the treatment plan. The combined detection of CD66b and PD-L1/PD-L2 is of significance to predict the prognosis of DLBCL patients.
V9302, an inhibitor of glutamine transport, suppresses proliferation and migration, and induces apoptosis in non-small cell lung cancer cells through ROS-mediated mTOR/p70S6K pathway.
Li S, Zhang X, Chen T … +6 more , Cong X, Feng W, Sun X, Zha C, Zhao S, Zhang P
Neoplasma · 2026 Jun · PMID 41987739 · Publisher ↗
This study aimed to investigate the effects and underlying mechanisms of V9302, an inhibitor of glutamine transport, on non-small cell lung cancer (NSCLC) cells. Proliferation was assessed using the cell counting kit-8,...
This study aimed to investigate the effects and underlying mechanisms of V9302, an inhibitor of glutamine transport, on non-small cell lung cancer (NSCLC) cells. Proliferation was assessed using the cell counting kit-8, colony formation, and EdU assays. Mitochondrial membrane potential was evaluated through JC-1 staining. Cell cycle distribution, apoptosis, and reactive oxygen species (ROS) levels were analyzed by flow cytometry, while migration was assessed using wound healing and Transwell assays. Western blotting was performed to determine protein expression levels. The antitumor efficacy of V9302 in vivo was evaluated using a xenograft mouse model with PC-9 cells. The results demonstrated that V9302 inhibited cell proliferation and induced G1-phase arrest in human lung adenocarcinoma PC-9 and A549 cells. Western blotting showed that V9302 significantly inhibited the ASCT2 protein expression in both PC-9 and A549 cells. Additionally, V9302 promoted apoptosis through a mitochondrial-dependent pathway, as evidenced by elevated levels of cleaved PARP, cleaved Caspase 3, cleaved Caspase 9, and Bax. V9302 also suppressed cell migration by downregulating N-cadherin and vimentin expression. Notably, V9302 triggered significant ROS accumulation and inhibited mTOR/p70S6K pathway activation, an effect that was partially restored by N-acetylcysteine, a ROS scavenger. Pretreatment with mTOR activator MHY1485 mitigated the inhibitory effects of V9302 on cell proliferation and migration, as well as its induction of apoptosis. Furthermore, V9302 inhibited tumor growth and induced apoptosis in a xenograft mouse model, without inducing detectable visceral toxicity. In conclusion, these findings demonstrate that V9302 reduces cell proliferation and migration, and causes apoptosis through the ROS-mediated mTOR/p70S6K pathway in NSCLC cells. These findings provide a novel theoretical foundation for advancing both academic and clinical research on NSCLC treatment.
Isoguanosine exerts anticancer effects in Huh-7 cells by modulating ROS-dependent MAPK and AKT signaling.
Wang AQ, Jin XY, Luo YH … +5 more , Wu N, Tang YJ, Liu YZ, Li TZ, Jin CH
Neoplasma · 2026 Jun · PMID 41987738 · Publisher ↗
Isoguanosine (ISO) is a naturally occurring bioactive compound with multiple pharmacological properties. In this study, the inhibitory effects of ISO on hepatocellular carcinoma (HCC) cells and its underlying molecular m...
Isoguanosine (ISO) is a naturally occurring bioactive compound with multiple pharmacological properties. In this study, the inhibitory effects of ISO on hepatocellular carcinoma (HCC) cells and its underlying molecular mechanisms were investigated. The cell viability after ISO treatment was assessed using the CCK-8 assay, trypan blue staining, and Hoechst 33342/PI double staining. The relevant targets of ISO and their regulatory mechanisms were predicted using network pharmacology and molecular docking technology. The induction of apoptosis by ISO on Huh-7 cells was detected by Annexin V-FITC/PI double staining combined with flow cytometry and western blotting. The cell cycle arrest effect of ISO on Huh-7 cells was detected by Ki-67 staining, flow cytometry, and western blotting. The migration-inhibition effect of ISO on Huh-7 cells was detected by the wound healing, Transwell, and western blotting. In addition, the effects of reactive oxygen species (ROS) and protein kinase B (AKT) on Huh-7 cells were investigated by using N-acetyl cysteine (NAC) and AKT inhibitor HY10249, respectively. Cell viability assays demonstrated that ISO exerts a significant cytotoxic effect on HCC cell lines. Network pharmacology analysis revealed that the core targets of ISO are associated with ROS, AKT, and mitogen-activated protein kinase (MAPK) signaling pathways. Molecular docking results indicate that ISO has a strong binding affinity for AKT1, CASP3, and GSK3B. Apoptosis assays indicated that ISO induces apoptosis in Huh-7 cells via the mitochondria-dependent pathway. Furthermore, ISO modulates apoptosis through the MAPK and signal transducer and activator of transcription 3 (STAT3) signaling pathways. Cell cycle assays showed that ISO induces G2/M phase arrest by elevating intracellular ROS levels. Migration assays demonstrated that ISO inhibits cell migration by regulating the AKT signaling pathway. In addition, pretreatment with NAC reversed ISO-induced apoptosis, cell cycle arrest, and inhibition of migration. ISO promotes apoptosis, induces cell cycle arrest, and inhibits Huh-7 cell migration. These findings provide a theoretical basis for further pharmacological research and support the potential development and application of ISO as an anticancer agent.
Prognostic model based on mitochondrial genes highlights ABCD3 as a potential therapeutic target in colorectal cancer.
Chen S, Li Y, Ding W … +7 more , Yin Y, Xin X, Wei X, Bao S, Pan B, Sun H, Xu M
Neoplasma · 2026 Jun · PMID 41987737 · Publisher ↗
Studies have shown that abnormal mitochondrial function is closely associated with the development and progression of colorectal cancer (CRC); however, prognostic models based on mitochondria-related genes are still lack...
Studies have shown that abnormal mitochondrial function is closely associated with the development and progression of colorectal cancer (CRC); however, prognostic models based on mitochondria-related genes are still lacking. We systematically analyzed the expression of mitochondrial-related genes in CRC patients and constructed and validated a mitochondrial gene risk prognostic model using various bioinformatics methods across the TCGA and GEO databases. We also investigated the effects of tumor microenvironment, immune cell infiltration, tumor mutation load, and drug sensitivity on patient prognosis. In addition, we overexpressed the ABCD3 gene using CRISPR-dCas9 technology and further explored the role of ABCD3 in cell proliferation and apoptosis by protein blotting and flow cytometry. The mitochondrial gene risk model was effective in predicting the prognosis of CRC patients, which showed that the high-risk group was significantly different from the low-risk group in terms of immune cell infiltration. Further analyses revealed a strong association between risk scores and clinicopathological features, immune infiltration, and drug sensitivity. We constructed a prognostic prediction model based on mitochondria-related genes and found that ABCD3 provides a novel biomarker for the individualized treatment of CRC.
CDH17 facilitates β-catenin nuclear translocation to reduce drug sensitivity in cisplatin-resistant gastric cancer cells.
Liu M, Han Z, Zhong Z … +6 more , Tan J, Zhu Q, Chen W, Huang S, Chen X, Tian X
Neoplasma · 2026 Apr · PMID 41866995 · Publisher ↗
Chemoresistance greatly impairs the effectiveness of chemotherapy in gastric cancer (GC) patients. According to our prior results, Cadherin-17 (CDH17) contributes to chemoresistance in GC through activating the Wnt/β-cat...
Chemoresistance greatly impairs the effectiveness of chemotherapy in gastric cancer (GC) patients. According to our prior results, Cadherin-17 (CDH17) contributes to chemoresistance in GC through activating the Wnt/β-catenin pathway; however, its specific molecular mechanisms require further elucidation. We compared the Wnt/β-catenin pathway activation levels between cisplatin (DDP)-resistant GC cell lines and their parental cell lines. Subsequently, we carried out loss-of-function and gain-of-function tests to investigate CDH17 for its effect on regulating β-catenin expression, nuclear transport, as well as transcriptional activity within DDP-resistant GC cells. Additionally, CDH17 was examined for its role in the expression of four ABC transporters using molecular assays. Finally, rescue experiments were carried out using the Wnt signaling pathway agonist CP21R7 and inhibitor IWR-1 to elucidate the specific mechanism of CDH17 in promoting chemotherapy resistance of GC cells. The results showed that the activation level of the Wnt/β-catenin signaling pathway was significantly elevated in DDP-resistant GC cell lines compared to their parental cell lines. Silencing CDH17 resulted in reduced expression, impaired nuclear translocation, and decreased transcriptional activity of β-catenin, whereas overexpression of CDH17 had the opposite effects. Notably, CDH17 was shown to specifically regulate the expression of ABCB1 (protein name: P-glycoprotein, P-gp) in resistant cells, with no observable impact on the other three ABC transporters (ABCC1, ABCG2, and ABCC2) examined. Importantly, treatment with IWR-1 effectively reversed the enhancing effect of CDH17 overexpression on P-gp protein expression, as well as its suppressive effects on DDP accumulation and chemosensitivity. Conversely, administration of CP21R7 attenuated the inhibitory consequences of CDH17 silencing on P-gp expression, DDP efflux, and drug resistance. In conclusion, CDH17 promotes the expression and nuclear translocation of β-catenin in GC cells, leading to activation of the Wnt/β-catenin signaling pathway, which subsequently upregulates ABCB1/P-gp expression and enhances cellular capacity for DDP efflux. These findings imply that targeting CDH17 could be a potential strategy for overcoming chemotherapy resistance in GC.
(-)-Guaiol inhibits lung cancer via PPARG-dependent fatty acid oxidation.
Zhao ZY, Zhang B, Luo YB … +6 more , Wang XY, Wang YL, Wang X, Tian JH, Wu JC, Li Y
Neoplasma · 2026 Apr · PMID 41866994 · Publisher ↗
The objective of this study was to explore the effect of (-)-guaiol on lung cancer using experimental validation, mRNA sequencing, and network pharmacology. Potential targets of (-)-guaiol and lung cancer were identified...
The objective of this study was to explore the effect of (-)-guaiol on lung cancer using experimental validation, mRNA sequencing, and network pharmacology. Potential targets of (-)-guaiol and lung cancer were identified through SwissTargetPrediction, TCMSP, PharmMapper, OMIM, GeneCards, and DisGeNET databases. Common targets were analyzed using PPI network, topological screening, and functional enrichment using STRING, Cytoscape, and Metascape. Molecular docking with core targets was performed, along with molecular dynamics. In vitro assays (cell counting kit-8 assay, colony formation, wound healing, Transwell, western blot) and in vivo studies (subcutaneous xenograft modeling in nude mice, immunohistochemistry, mRNA sequencing) were conducted to validate the anti-tumor effects and mechanisms of (-)-guaiol compared with the control group. Through multi-database prediction, 153 (-)-guaiol targets and 91 common lung cancer targets were identified. Protein-protein interaction (PPI) network analysis screened 21 core targets (including ESR1, EGFR, etc.). GO and KEGG enrichment analyses revealed that these targets are involved in the regulation of pathways such as fatty acid metabolism. Molecular docking and molecular dynamics results demonstrated that (-)-guaiol possessed a favorable binding affinity toward the target proteins SRC, PTGS2, GSK3B, PPARG, ESR1, and HSP90AA1. mRNA sequencing indicated that the gene expression levels of both PPARG and CD36 were downregulated in lung cancer tissues of mice treated with (-)-guaiol compared with the control group. Combining the results of molecular docking, molecular dynamics, and mRNA sequencing, we selected the PPARG-related signaling pathway for subsequent experiments. Both in vivo and in vitro experiments validated that (-)-guaiol inhibits lung cancer cell proliferation, invasion, and xenograft tumor growth in mice by downregulating the PPARG pathway. To conclude, our results demonstrated that (-)-guaiol suppresses lung cancer progression through downregulation of the fatty acid oxidation-related pathway mediated by PPARG.
Research progress on the role of DDR1 in cancer and targeted therapy strategy.
Guan X, Zhang Y, Guan X … +1 more , Yan H
Neoplasma · 2026 Apr · PMID 41709753 · Publisher ↗
Discoidin domain receptor 1 (DDR1) is a receptor tyrosine kinase activated by various types of collagen. Abnormal activation of DDR1 is closely related to the occurrence and development of solid tumors and plays an impor...
Discoidin domain receptor 1 (DDR1) is a receptor tyrosine kinase activated by various types of collagen. Abnormal activation of DDR1 is closely related to the occurrence and development of solid tumors and plays an important role in the regulation of cell adhesion, survival, proliferation, migration, and invasion. Thus, DDR1 is a promising therapeutic target in the field of oncology. This review introduces the structural characteristics of DDR1, focusing on its role in tumor progression and related signaling pathways. It also explores the relationship between DDR1 and tumor chemotherapy resistance, and elaborates on the current research status and development prospects for inhibitors and antibodies targeting DDR1. Thus, the DDR1 inhibition strategy may serve as a new alternative for treating cancer patients.
Cell surface topography differs in the human "glia-like" and glioma cultures.
Sivakova I, Lorencova M, Perzelova A … +2 more , Galfiova P, Polak S
Neoplasma · 2026 Apr · PMID 41709752 · Publisher ↗
Glioblastoma multiforme is the most malignant and incurable primary brain tumor. Infiltrative growth of gliomas into surrounding brain tissue may cause the presence of normal cells in glioma cultures. The aim of this stu...
Glioblastoma multiforme is the most malignant and incurable primary brain tumor. Infiltrative growth of gliomas into surrounding brain tissue may cause the presence of normal cells in glioma cultures. The aim of this study is to develop a simple, rapid method for detecting normal cells in short-term glioma cultures, to be applied primarily to personalized glioma treatment. Cell lines with permanent cell growth consist solely of cancer cells. Here, we examined two glioblastoma cell lines (8-MG-BA and 170-MG-BA), one brain metastatic carcinoma cell line (135-BCA), five short-term glioblastomas, and five human "glia-like" cultures using scanning electron microscopy (SEM), standard phase contrast microscopy, and GFAP immunofluorescence. All cells in glioblastoma and carcinoma cell lines were covered with microvilli of varying density, 4/5 of short-term glioblastoma cultures contained 1-3% cells with sparse microvilli, and one culture (139-GBM) showed microvilli in 15-20% of the cells and a higher percentage of GFAP-positive cells. A rare occurrence (less than 1%) of cells bearing microvilli was observed in all "glia-like" cultures. Using SEM, we observed similar cells with microvilli in both glioblastoma cell lines, but in the 135-BCA line, the microvilli were significantly shorter. Microvilli rarely occurred on normal "glia-like" cells. Based on this observation, we conclude that our 4/5 of short-term glioblastoma cultures contain predominantly normal "glia-like" cells. SEM could be a valuable method for distinguishing normal and tumor cells in short-term glioblastoma cultures, which have similar morphologies at light microscopy and immunophenotypes. We conclude that microvilli are characteristic of a specific tumor cell surface topography compared to "glia-like" cells.
SLC44A1 promotes AML progression and chemoresistance by regulating the Notch signaling pathway.
Cao S, Pan C, Hu X … +4 more , Hu T, Li Y, Fang Q, Wang J
Neoplasma · 2026 Feb · PMID 41568897 · Publisher ↗
Despite advances in treatment, acute myeloid leukemia (AML) remains a formidable therapeutic challenge, highlighting the urgent need for novel biomarkers and therapeutic targets. The choline transporter SLC44A1 has been...
Despite advances in treatment, acute myeloid leukemia (AML) remains a formidable therapeutic challenge, highlighting the urgent need for novel biomarkers and therapeutic targets. The choline transporter SLC44A1 has been implicated in cancer progression; however, its role in AML remains largely unexplored. Here, we investigated the clinical relevance and molecular mechanisms of SLC44A1 in AML. Analysis of The Cancer Genome Atlas (TCGA) datasets revealed significant upregulation of SLC44A1 in AML patients, correlating with poor patient prognosis. Functional studies demonstrated that SLC44A1 knockdown markedly inhibited AML cell proliferation and enhanced chemosensitivity to cytarabine and venetoclax. RNA sequencing and pathway analysis identified the NOTCH signaling pathway as a key downstream target of SLC44A1, which was further validated by western blot. Collectively, our findings establish SLC44A1 as a crucial regulator of AML progression and chemoresistance, highlighting its dual potential as a prognostic biomarker and a therapeutic target.
Prognostic value and clinical significance of tumoral PD-L1 and stromal α-SMA expression in diffuse pleural mesothelioma.
Sun Y, Li L, Cai L … +4 more , Yang J, Qian J, Wang F, Wang L
Neoplasma · 2026 Feb · PMID 41568896 · Publisher ↗
Diffuse pleural mesothelioma (PM) is a rare malignant neoplasm with an extremely poor prognosis. Prognostic assessment remains challenging, highlighting the urgent need for reliable biomarkers to guide precise and effect...
Diffuse pleural mesothelioma (PM) is a rare malignant neoplasm with an extremely poor prognosis. Prognostic assessment remains challenging, highlighting the urgent need for reliable biomarkers to guide precise and effective therapy. Programmed death ligand 1 (PD-L1) has been suggested as a predictive biomarker for PM, but existing data are limited and controversial. Although advances have been made in understanding cancer-associated fibroblasts (CAFs) within the PM tumor microenvironment, their clinical and prognostic significance remains poorly elucidated. A retrospective analysis of 51 pathologically diagnosed PM was performed. We evaluated clinicopathological factors (including tumoral PD-L1, stromal α-SMA, and Ki-67 percentage by immunohistochemistry) and analyzed their correlation with overall survival (OS) using Kaplan-Meier and multivariate Cox regression. A total of 12 potential prognostic factors were evaluated in the univariate analysis, and 6 factors were found to be significantly associated with a poor prognosis in PM patients. Multivariate analysis identified histological classification, TNM stage, and PD-L1 expression as independent prognostic factors in PM patients. Stromal α-SMA positivity, a marker of poor prognosis, was significantly correlated with male, non-epithelioid subtype, and a high Ki-67 index. Moreover, α-SMA positivity tended to show an increased likelihood of PD-L1 expression (p=0.065). The expression of tumor PD-L1 could serve as an adverse prognostic factor for PM patients. Its potential association with tumor stromal α-SMA expression warrants further investigation, particularly in the context of unmet needs in tumor immunotherapy.
DNA methylation-predicted GDF-15 and mortality in cancer survivors: a cohort study.
Nong J, Shi K, Zhang Y
Neoplasma · 2026 Feb · PMID 41568895 · Publisher ↗
Developing non-invasive prognostic biomarkers remains critical to improving personalized cancer care. Growth differentiation factor-15 (GDF-15), a TGF-β family cytokine, plays a key role in tumorigenesis and immune evasi...
Developing non-invasive prognostic biomarkers remains critical to improving personalized cancer care. Growth differentiation factor-15 (GDF-15), a TGF-β family cytokine, plays a key role in tumorigenesis and immune evasion. Circulating GDF-15 serves as a biomarker for cancer prognosis, and DNA methylation (DNAm)-predicted GDF-15 has been linked to mortality risk in the general population. However, the association between DNAm-predicted GDF-15 and mortality risk in cancer survivors remains unexplored. We analyzed the association between DNAm-predicted GDF-15 and all-cause, long-term all-cause, and cancer mortality risks using a cohort of 343 cancer survivors from the National Health and Nutrition Examination Survey (NHANES) 1999-2002 with a median follow-up of 138 months. Multivariable Cox regression reporting hazard ratios (HRs) and 95% confidence intervals (CIs) demonstrated that each 1-standard deviation (SD) increment in DNAm-predicted GDF-15 was associated with a 60% higher all-cause mortality risk adjusted with model 1 of age and sex, and a 54% greater all-cause mortality risk in model 2 adjusted additionally for ethnicity, education, smoking, and coronary heart disease. Participants in the high GDF-15 tertile showed a 201% and 166% higher mortality risk in model 1 and model 2, respectively (both p for trend <0.0001) compared to the low tertile. Its association with long-term mortality risk remains unchanged. Stratified analyses indicated consistent relationships across multiple subgroups. Kaplan-Meier and competing risk analyses revealed a graded increase in cancer mortality risk across ascending GDF-15 tertiles; Cox models confirmed a significant positive association per 1-SD increment in the unadjusted model and model 1, which remained consistent in direction and magnitude in model 2, with a marginally significant (p=0.052). The current study provided evidence that DNAm-predicted GDF-15, an alternative and precise estimate of GDF-15 based on DNA methylation, is positively associated with all-cause and long-term all-cause mortality risks and showed a trend of positive association with cancer mortality among cancer survivors. Future larger longitudinal studies with serial DNAm-predicted GDF-15 assessments are needed to verify potential causal links.
Treatment-Related Toxicity of the BEAM/BeEAM Conditioning Regimen in Patients Undergoing Autologous Hematopoietic Stem Cell Transplantation.
Kašperová B, Mego M, Čierniková S … +6 more , Ladická M, Rusiňáková Z, Ševčíková A, Kašperová S, Vranovský A, Drgoňa Ľ
Neoplasma · 2025 Dec · PMID 41567023 · Publisher ↗
Conditioning regimens prior to hematopoietic stem cell transplantation (HSCT) are highly intensive and associated with significant toxicity, which can influence survival and quality of life. This study aimed to analyze t...
Conditioning regimens prior to hematopoietic stem cell transplantation (HSCT) are highly intensive and associated with significant toxicity, which can influence survival and quality of life. This study aimed to analyze the incidence of gastrointestinal, hematological toxicity, changes in quality of life, and cognitive functions in lymphoma patients undergoing autologous HSCT with BEAM/BeEAM conditioning. A total of 27 lymphoma patients indicated for autologous HSCT were enrolled in this prospective observational study from January 2020 to August 2023. Data collection was performed at admission and at the end of hospitalization, prior to discharge. Monitored parameters included laboratory tests (hematology and biochemistry), patient-reported quality of life assessed using the QLQ-C30 questionnaire, and perceived cognitive function evaluated using the FACT-Cog questionnaire. Mucositis of any grade occurred in 25 patients (92.6%), with diarrhea being the most common gastrointestinal symptom (any grade 85.2%, grade 3-4 37.0%). Diarrhea severity was generally independent of age, baseline blood counts, engraftment, weight loss, or hospitalization, except for an association between severe diarrhea and lower pre-transplant TSH (p=0.03). All patients experienced grade 1-2 weight loss, and 81.5% developed febrile neutropenia. Quality of life declined during transplantation, notably in role functioning, social functioning, and cognitive performance, alongside worsening fatigue, nausea/vomiting, pain, appetite loss, and diarrhea (all p-values <0.05). FACT-Cog scores showed no significant cognitive decline. The 2-year overall survival was 92.1% (95% CI 81.6-100%), while patients with SII >520.81 had lower survival (82.5%, 95% CI 60.4-100%, p=0.04), with higher SII significantly associated with worse outcomes. Autologous transplantation and the BEAM/BeEAM conditioning regimen are associated with considerable mucosal and hematologic toxicity. Patients are at risk of infections, nutritional deficits due to reduced intake, and deterioration in quality of life.
PAF15 drives melanoma progression by promoting proliferation concomitant with suppression of DNA damage and apoptosis: a novel therapeutic vulnerability.
Ji Y, Li C, Hao H … +6 more , Liu Y, Mao Y, Guo L, Liu L, Liu Y, Shi S
Neoplasma · 2025 Dec · PMID 41567022 · Publisher ↗
PAF15 is an oncogene and is overexpressed across multiple malignancies. However, its biological role in melanoma remains largely unclear. In this research, bioinformatics analysis (GEPIA2, TCGA, CancerSEA) confirmed tran...
PAF15 is an oncogene and is overexpressed across multiple malignancies. However, its biological role in melanoma remains largely unclear. In this research, bioinformatics analysis (GEPIA2, TCGA, CancerSEA) confirmed transcriptional PAF15 overexpression in melanoma, correlating with a poor prognosis and implicating pathways involved in cell cycle, proliferation, DNA damage, and repair. Immunohistochemical analysis further confirmed high expression of PAF15 protein in clinical melanoma tissues. Subsequently, the impact of PAF15 on melanoma cell proliferation and cell cycle progression was quantified through MTT assay and propidium iodide staining. Annexin V staining and immunofluorescence were used to assess apoptosis and DNA damage. Markers associated with these biological pathways were evaluated by western blot. Evaluation of PAF15-mediated tumorigenic effects was performed using a subcutaneous xenograft model. The results revealed that PAF15 knockdown markedly suppressed melanoma cell proliferation through the induction of G0/G1 phase cell cycle arrest. Additionally, PAF15 knockdown triggered genomic instability, as evidenced by increased DNA damage markers, and promoted caspase-dependent apoptosis. Furthermore, PAF15 knockdown suppressed the growth of xenograft tumors in vivo. Notably, these tumor-inhibiting effects of PAF15 knockdown were effectively rescued upon PAF15 reconstitution. Summed up, these findings establish PAF15 as both a prognostic indicator for unfavorable clinical outcomes and a promising therapeutic vulnerability in melanoma.
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