International Journal Of Oncology[JOURNAL]
Sun
200 papers
Curcumin inhibits the activity of ubiquitin ligase Smurf2 to promote NLRP3‑dependent pyroptosis in non‑small cell lung cancer cells.
Xi Y, Zeng S, Tan X … +1 more , Deng X
Int J Oncol · 2025 Mar · PMID 39950328 · Full text
Non‑small cell lung cancer (NSCLC) is a malignant tumor of significant clinical relevance. Curcumin has been investigated for its potential anticancer properties, as it has been reported to act through multiple cancer‑re...
Non‑small cell lung cancer (NSCLC) is a malignant tumor of significant clinical relevance. Curcumin has been investigated for its potential anticancer properties, as it has been reported to act through multiple cancer‑related targets and pathways. The present study aimed to explore the effects of curcumin in NSCLC using both and models. NSCLC cell lines (specifically, A549 and NCI‑H1299 cells), and a mouse tumor model established through the subcutaneous injection of A549 cells, were utilized to evaluate the effects of curcumin intervention. The effects of treatment with curcumin on NOD‑like receptor pyrin domain‑containing 3 (NLRP3) ubiquitination, cell pyroptosis and pyroptosis‑associated factors were also evaluated. In addition, Smad ubiquitination regulatory factor 2 (Smurf2) was analyzed via a series of knockdown and overexpression experiments, both and , aimed at investigating its association with curcumin and NLRP3. The results obtained from these experiments showed that curcumin inhibited NSCLC cell growth, promoted pyroptosis and reduced the level of NLRP3 ubiquitination. NLRP3 knockdown reversed the curcumin‑induced increase in pyroptosis‑associated factors both and . Additionally, Smurf2 interacted with NLRP3 and alterations in Smurf2 expression levels influenced NLRP3 ubiquitination and cell pyroptosis. Moreover, molecular docking analysis demonstrated that curcumin could bind directly to Smurf2, which subsequently led to an inhibition of Smurf2 activity. Knockdown of Smurf2 enhanced curcumin's ability to stabilize NLRP3 and to promote pyroptosis, whereas Smurf2 overexpression negated these effects. In the animal model, curcumin treatment led to reduced tumor volumes and weights, in addition to a decreased expression level of Ki67 and increased expression levels of NLRP3 and pyroptosis‑associated factors. Similarly, these effects were enhanced or reversed by Smurf2 knockdown or overexpression, respectively. In conclusion, the findings of the present study showed that curcumin inhibited Smurf2 activity, thereby promoting NLRP3‑dependent pyroptosis in NSCLC cells. In addition, these findings have provided mechanistic insights into the role of curcumin in NSCLC, opening an avenue for its potential therapeutic application.
Long non‑coding RNA ABHD11‑AS1 inhibits colorectal cancer progression through interacting with EGFR to suppress the EGFR/ERK signaling pathway.
Tan S, Li S, Xia L … +15 more , Jiang X, Ren Z, Peng Q, Peng M, Yang W, Xu X, Oyang L, Shen M, Wang J, Li H, Wu N, Tang Y, Liao Q, Lin J, Zhou Y
Int J Oncol · 2025 Mar · PMID 39950321 · Full text
Long non‑coding (lnc)RNAs participate in colorectal cancer (CRC) occurrence and progression. The present study aimed to investigate whether lncRNA ABHD11‑AS1 regulates malignant biological behavior of CRC cells. Bioinfor...
Long non‑coding (lnc)RNAs participate in colorectal cancer (CRC) occurrence and progression. The present study aimed to investigate whether lncRNA ABHD11‑AS1 regulates malignant biological behavior of CRC cells. Bioinformatic analysis, reverse transcription‑quantitative PCR and hybridization revealed that ABHD11‑AS1 expression was decreased in CRC samples and associated with an unfavorable prognosis. ABHD11‑AS1 overexpression significantly decreased proliferation, migration and invasion of CRC cells, whereas ABHD11‑AS1 inhibition had the opposite effects. ABHD11‑AS1 interacted with EGFR to inhibit EGFR phosphorylation and attenuate EGFR/ERK signaling, which in turn suppressed the malignant biological behavior of CRC cells. The tumor suppressor function of ABHD11‑AS1 was attenuated by the EGFR agonist NSC228155. Finally, resveratrol (RSV) inhibited CRC cell proliferation, migration and invasion, which may be associated with RSV‑induced decrease in SPT6 homolog, histone chaperone and transcription elongation factor protein expression and increase in ABHD11‑AS1 transcript levels. ABHD11‑AS1 inhibited the phosphorylation of EGFR and decreased EGFR/ERK signaling by interacting with EGFR, thereby delaying the progression of CRC. The ABHD11‑AS1/EGFR/ERK axis may be a novel therapeutic target for preventing CRC progression.
[Corrigendum] Upregulated NTF4 in colorectal cancer promotes tumor development via regulating autophagy.
Yang Z, Chen Y, Wei X … +3 more , Wu D, Min Z, Quan Y
Int J Oncol · 2025 Mar · PMID 39950318 · Full text
Following the publication of the above article, the authors subsequently realized that, during the process of collating the raw data, Fig. 1 [the immunohistochemical (IHC) results for stage IV colorectal cancer (CRC)], F...
Following the publication of the above article, the authors subsequently realized that, during the process of collating the raw data, Fig. 1 [the immunohistochemical (IHC) results for stage IV colorectal cancer (CRC)], Fig. 2A (the control β‑actin blots) and Fig. 5C and D (both the images selected for the clone formation assays, and the histograms showing the quantification of the data) were inadvertently assembled incorrectly. These errors arose as a consequence of the affected files having been named similarly to those of the correct panels. The revised versions of Figs. 1, 2 and 5, now featuring the correct IHC data for stage IV CRC in Fig. 1, the correct control western blots in Fig. 2 and the correct colony formation assay data (and quantification thereof) in Fig. 5, are shown on the next three pages. Note that the correction of these figures does not affect the key findings of the study (either the existing published results or the conclusions reached from the results). The authors thank the Editor of for granting them the opportunity to publish this corrigendum. All the authors agree with the publication of this corrigendum; furthermore, they apologize to the readership of the journal for any inconvenience caused. [International Journal of Oncology 56: 1442‑1454, 2020; DOI: 10.3892/ijo.2020.5027].
Pathogenetic development, diagnosis and clinical therapeutic approaches for liver metastasis from colorectal cancer (Review).
Jin Z, Li Y, Yi H … +5 more , Wang M, Wang C, Du S, Zeng W, Zong Z
Int J Oncol · 2025 Mar · PMID 39950314 · Full text
Colorectal cancer (CRC) is a prevalent malignancy and a significant proportion of patients with CRC develop liver metastasis (CRLM), which is a major contributor to CRC‑related mortality. The present review aimed to comp...
Colorectal cancer (CRC) is a prevalent malignancy and a significant proportion of patients with CRC develop liver metastasis (CRLM), which is a major contributor to CRC‑related mortality. The present review aimed to comprehensively examine the pathogenetic development and diagnosis of CRLM and the clinical therapeutic approaches for treatment of this disease. The molecular mechanisms underlying CRLM were discussed, including the role of the tumour microenvironment and epithelial‑mesenchymal transition. The present review also highlighted the importance of early detection and the current challenges in predicting the development of CRLM. Various treatment strategies were reviewed, including surgical resection, chemotherapy and immunotherapy, and the potential of novel therapies, such as selective internal radiation therapy and Traditional Chinese Medicine. Despite recent advancements in treatment options, the treatment of CRLM remains a therapeutic challenge due to the complexity of the liver microenvironment and the heterogeneity of CRC. The present review emphasized the need for a multidisciplinary approach and the integration of emerging therapies to improve patient outcomes.
Norchelerythrine from (Thunb.) Pers. promotes differentiation and apoptosis by activating DNA damage response in acute myeloid leukemia.
Lee JE, Jeon BE, Kwon CS … +6 more , Kim HY, Kim TJ, Seo Y, Lee SH, Shin HJ, Kim SW
Int J Oncol · 2025 Mar · PMID 39918000 · Full text
Acute myeloid leukemia (AML) is the most prevalent form of leukemia in adults. The cornerstone of first‑line chemotherapy for AML has poor survival rates, underscoring the urgent need for development of novel therapeutic...
Acute myeloid leukemia (AML) is the most prevalent form of leukemia in adults. The cornerstone of first‑line chemotherapy for AML has poor survival rates, underscoring the urgent need for development of novel therapeutic agents. Differentiation therapy targets the blockade of differentiation in myeloid progenitor cells. The present study screened 100 plant extracts native to South Korea to search for those with differentiation‑inducing activity in AML. Differentiation‑inducing activity was assessed by measuring CD11b expression using fluorescence activated cell sorting. Of these, (Thunb.) Pers. (CIP) exhibited the highest efficacy. CIP induced myeloid differentiation, decreased viability and increased cell apoptosis and cell cycle arrest in HL‑60, U937 and THP‑1 cells. Furthermore, ultra‑performance liquid chromatography‑quadrupole time‑of‑flight mass spectrometry identified norchelerythrine as the primary anti‑leukemic compound in CIP. Norchelerythrine induced differentiation and promoted cell cycle arrest and apoptosis, mirroring the tumor‑suppressive effects of CIP, and notably decreased cell viability in patients with various genetic abnormalities. The present mechanistic study showed that norchelerythrine stimulated reactive oxygen species generation, leading to activation of DNA damage signaling and upregulation of p21, a cyclin‑dependent kinase inhibitor. Overall, norchelerythrine isolated from CIP may be a novel therapeutic option in AML.
[Retracted] Zinc finger protein‑like 1 is a novel neuroendocrine biomarker for prostate cancer.
Masud N, Aldahish A, Iczkowski KA … +2 more , Kale A, Shah GV
Int J Oncol · 2025 Mar · PMID 39917995 · Full text
Following the publication of this paper, a concerned reader drew to the attention of the Editorial Office that, for the photomicrographs shown in Fig. 2B on p. 8, the same image had apparently been selected to represent...
Following the publication of this paper, a concerned reader drew to the attention of the Editorial Office that, for the photomicrographs shown in Fig. 2B on p. 8, the same image had apparently been selected to represent the images for cerebrum and cerebellum from the brain. Secondly, the same image for the prostate tissue in Fig. 2B was used as the 'Matched normal' data in Fig. 3C on p. 9, and thirdly, the si3 and si3+CT images selected for Fig. 7B on p. 13 appeared to be derived from the same original source. Finally, after having performed an independent analysis of the data in the Editorial Office, it was noted that, for the wound healing assay data shown in Fig. 8E on p. 14, overlapping sections were identified comparing the CT and Overexp panels in the lower panel of images in this figure, such that data which were intended to show the results of differently performed experiments had apparently been derived from the same original source. After having considered these issues, owing to the number of instances of apparently misassembled data that have been identified in this paper, and also on the basis of an overall lack of confidence in the presented data, the Editor of has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [International Journal of Oncology 62: 38, 2023; DOI: 10.3892/ijo.2023.5486].
Unleashing the power of urine‑based biomarkers in diagnosis, prognosis and monitoring of bladder cancer (Review).
Wan X, Wang D, Zhang X … +4 more , Xu M, Huang Y, Qin W, Chen S
Int J Oncol · 2025 Mar · PMID 39917986 · Full text
Bladder cancer (BCa) is a prevalent malignant neoplasm of the urinary tract with high incidence rate, frequent recurrence and rapid disease progression. Conventional approaches for diagnosing, prognosticating and monitor...
Bladder cancer (BCa) is a prevalent malignant neoplasm of the urinary tract with high incidence rate, frequent recurrence and rapid disease progression. Conventional approaches for diagnosing, prognosticating and monitoring BCa often rely on invasive procedures such as cystoscopy and tissue biopsy, which are associated with high costs and low patient compliance for follow‑up. Liquid biopsies have advantages, such as being non‑invasive, real‑time, and reproducible, in obtaining diverse biomarkers derived from cellular, molecular, proteomic and genetic signatures in urine or plasma samples. Although plasma‑based biomarkers have been clinically validated, urine provides greater specificity for directly assessing biological materials from urological sources. The present review summarizes advancements and current limitations in urinary protein, genetic and epigenetic biomarkers for disease progression and treatment response of BC, compares performance and application scenarios of urine and blood biomarkers and explores how urinary biomarkers may serve as an alternative or complementary tool to traditional diagnostic methods. The integration of urine‑based or plasma‑based biomarkers into existing diagnostic workflows offers promising avenues for improving accuracy and efficiency of diagnosis in the management of BCa. Notably, the emergence of synthetic biomarkers and urine metabolites, combined with artificial intelligence or bioinformatic technologies, has promise in the screening of potential targets. Continued research and validation efforts are needed to translate these findings into routine clinical practice, ultimately improving patient outcomes and decreasing the burden of BCa.
circ_0004662 contributes to colorectal cancer progression by interacting with hnRNPM.
Zhang Y, Wang J, Quan R … +1 more , Lyu L
Int J Oncol · 2025 Feb · PMID 39821691 · Full text
Circular (circ)RNAs participate in colorectal cancer (CRC) occurrence and progression. However, the role of hsa_circ_0004662 (circ_0004662) in CRC remains unknown. Reverse transcription‑quantitative PCR noted high expres...
Circular (circ)RNAs participate in colorectal cancer (CRC) occurrence and progression. However, the role of hsa_circ_0004662 (circ_0004662) in CRC remains unknown. Reverse transcription‑quantitative PCR noted high expression of circ_0004662 in CRC compared with normal colorectal epithelial cells. circ_0004662 knockdown inhibited migration of CRC cells and ; would healing and Transwell assays showed that circ_0004662 overexpression contributed to CRC migration. Nuclear cytoplasmic analysis and fluorescence hybridization revealed localization of circ_0004662 in the nucleus and cytoplasm. CircRNADB databases predicted that circ_0004662 exhibited translational potential and liquid chromatography‑mass spectrometry (LC‑MS) of circ_0004662 pull‑down products suggested that circ_0004662 bound to multiple ribosomal subunits. However, peptide products of 149aa translated by circ_0004662, with a molecular weight of ~17 kDa were not detected. Nevertheless, LC‑MS analysis indicated that circ_0004662 bound multiple proteins. Immunoprecipitation of RNA‑binding proteins revealed that circ_0004662 bound to heterogeneous nuclear ribonucleoprotein M (hnRNPM) and that hnRNPM interference decreased circ_0004662 expression, thereby affecting CRC progression. In summary, circ_0004662 was significantly upregulated in CRC. As a non‑coding RNA, it may promote CRC progression by binding to hnRNPM, which may serve as a potential target for treating CRC.
SLC25A1 promotes lymph node metastasis of esophageal squamous cell carcinoma by regulating lipid metabolism.
Zhang G, Wu J, Ji M … +2 more , Liu X, Shi M
Int J Oncol · 2025 Feb · PMID 39821659 · Full text
Solute carrier family 25 member 1 (SLC25A1) affects lipid metabolism and energy regulation in multiple types of tumor cell, affecting their proliferation and survival. To the best of our knowledge, however, the impact of...
Solute carrier family 25 member 1 (SLC25A1) affects lipid metabolism and energy regulation in multiple types of tumor cell, affecting their proliferation and survival. To the best of our knowledge, however, the impact of SLC25A1 on the proliferation and survival of esophageal squamous cell carcinoma (ESCC) cells has yet to be explored. Here, SLC25A1 expression was detected in ESCC tissues and cell lines. SLC25A1 was silenced or blocked by lentivirus transfection or 2‑[(4‑chloro‑3‑nitrophenyl)sulfonylamino]benzoic acid in ESCC cells. To evaluate the impact of SLC25A1 on and proliferation, invasion and migration of ESCC cells, Cell Counting‑Kit, wound healing, colony formation, Transwell, EdU, flow cytometry, tumor xenograft in nude mice, lipid metabolism and energy metabolism detection assays were performed. Reverse transcription‑quantitative PCR and western blot analysis were performed to determine expression of downstream molecules and pathway proteins following the silencing and blockade of SLC25A1. SLC25A1 was significantly overexpressed in ESCC tissue and cell lines. The targeted silencing of SLC25A1 or inhibition of its protein led to a significant decrease in proliferative, invasive and migratory capabilities of ESCC cells, accompanied by increased apoptosis. Additionally, silencing of the SLC25A1 gene significantly inhibited xenograft tumor growth . The present results indicate that knockdown or blockade of SLC25A1 can significantly impede the malignant biological behavior of ESCC.
Exploring the antiproliferative effect of PI3K/Akt/mTOR pathway and CDK4/6 inhibitors in human papillomavirus‑positive and ‑negative head and neck squamous cell carcinoma cell lines.
Verhees F, Demers I, Legemaate D … +4 more , Jacobs R, Hoeben A, Kremer B, Speel EJ
Int J Oncol · 2025 Feb · PMID 39791215 · Full text
Human papillomavirus (HPV)‑positive and -negative head and neck squamous cell carcinoma (HNSCC) are often associated with activation of the phosphatidylinositol 3‑kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) pa...
Human papillomavirus (HPV)‑positive and -negative head and neck squamous cell carcinoma (HNSCC) are often associated with activation of the phosphatidylinositol 3‑kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) pathway due to mutations or amplifications in , loss of or activation of receptor tyrosine kinases. In HPV‑negative tumors, (encoding p16 protein) inactivation or (encoding Cyclin D1 protein) amplification frequently results in sustained cyclin‑dependent kinase (CDK) 4/6 activation. The present study aimed to investigate the efficacy of the CDK4/6 inhibitors (CDKi) palbociclib and ribociclib, and the PI3K/Akt/mTOR pathway inhibitors (PI3Ki) gedatolisib, buparlisib and alpelisib, in suppressing cell viability of HPV‑positive and ‑negative HNSCC cell lines. Inhibitor efficacy was assessed using MTT assay and western blotting analysis. Cell cycle analysis was performed using flow cytometry and apoptosis was assessed using annexin V staining. Metabolic changes in terms of glycolysis and oxidative metabolism were measured by Seahorse XF96 extracellular Flux analysis. The results of the present study showed that both HPV‑positive and ‑negative HNSCC cell lines were sensitive to PI3Ki. In general, PI3Ki decreased PI3K/Akt/mTOR pathway activity, resulting in apoptosis, and decreased oxidative and glycolytic metabolism. The CDKi were particularly effective in blocking HPV‑negative cell line viability, showing decreased retinoblastoma expression and G1‑phase cell cycle arrest, whereas apoptosis was not induced. Thus, PI3Ki and CDKi efficiently inhibited their respective pathways and HNSCC cell viability , with the latter occurring only in HPV‑negative cell lines. Whereas PI3Ki induced apoptosis and attenuated cellular metabolism, CDKi led to cell cycle arrest. Further research should be performed to elucidate whether (a combination of) these inhibitors may be effective therapeutic agents for patients with HNSCC.
LGR4 promotes proliferation and homing via activation of the NF‑κB signaling pathway in multiple myeloma.
He N, Yang Q, Li Z … +10 more , Guo J, Kuang C, Zhu Y, Liu X, Chen X, Shi F, Feng X, An G, Zhang G, Zhou W
Int J Oncol · 2025 Feb · PMID 39749708 · Full text
Multiple myeloma (MM) is a plasma cell malignancy characterized by clonal proliferation in the bone marrow (BM). Previously, it was reported that G‑protein‑coupled receptor 4 (LGR4) contributed to early hematopoiesis and...
Multiple myeloma (MM) is a plasma cell malignancy characterized by clonal proliferation in the bone marrow (BM). Previously, it was reported that G‑protein‑coupled receptor 4 (LGR4) contributed to early hematopoiesis and was associated with poor prognosis in patients with MM. However, the mechanism of cell homing and migration, which is critical for MM progression, remains unclear. In the present study, cell counting, cell cycle and BrdU assays were performed to evaluate cell proliferation. Transwell assay and Xenograft mouse models were performed to evaluate cell migration and homing ability both and . I was found that overexpression of LGR4 promotes MM cell adhesion, migration and homing to BM both , while exacerbating osteolytic bone destruction . However, the LGR4 knockdown displayed the opposite effect. Further mechanistic studies demonstrated that LGR4 activated the nuclear factor kappa B (NF‑κB) signaling pathway and migration‑related adhesion molecule, thus promoting MM cell homing. Moreover, inhibiting the NF‑κB pathway was found to suppress MM cell homing. These findings identify LGR4 as a critical regulator of myeloma cell migration, homing and tumorigenesis, offering a potential therapeutic strategy for MM treatment.
[Retracted] Differential effects of PXD101 (belinostat) on androgen-dependent and androgen-independent prostate cancer models.
Gravina GL, Marampon F, Giusti I … +7 more , Carosa E, Di Sante S, Ricevuto E, Dolo V, Tombolini V, Jannini EA, Festuccia C
Int J Oncol · 2025 Feb · PMID 39749699 · Full text
Following the publication of the above article, a concerned reader drew to the Editor's attention that certain of the western blot assay data shown in Fig. 4G on p. 717 were strikingly similar to data that had appeared i...
Following the publication of the above article, a concerned reader drew to the Editor's attention that certain of the western blot assay data shown in Fig. 4G on p. 717 were strikingly similar to data that had appeared in a paper published previously in the journal , which had been written by different authors at different research institutes. Moreover, there appeared to be as many as five sets of duplicated protein bands in Fig. 4B and C, including the appearance of apparently the same protein band in different orientations in Fig. 4C in one case, and certain data shown in Fig. 4B and G had apparently been re-used in these figure parts. After having performed an independent assessment of these issues in the Editorial Office, these concerns of the reader were found to have been validated; therefore, the Editor of has decided that this paper should be retracted from the publication. After having been in contact with the authors, they accepted the decision to retract the paper. The corresponding author, Claudio Festuccia, takes full responsibility for the raised concerns and clarifies that the other co-authors were not directly involved in the preparation of the submitted figures. The Editor apologizes to the readership for any inconvenience caused. [International Journal of Oncology 40: 711-720, 2012; DOI: 10.3892/ijo.2011.1270].
SUCLG1 promotes aerobic respiration and progression in plexiform neurofibroma.
Zhou Z, Li Q, Huo R
Int J Oncol · 2025 Feb · PMID 39749698 · Full text
Plexiform neurofibromas (PNFs) are benign tumors that affect 20‑50% of patients with type I neurofibromatosis (NF1). PNF carries a risk of malignancy. There is no effective cure for PNF. Its onset may be associated with...
Plexiform neurofibromas (PNFs) are benign tumors that affect 20‑50% of patients with type I neurofibromatosis (NF1). PNF carries a risk of malignancy. There is no effective cure for PNF. Its onset may be associated with genetic and metabolic abnormalities, but the exact mechanisms remain unclear. Succinate‑CoA ligase GDP/ADP‑Forming Subunit α(SUCLG1), a catalytic enzyme in the tricarboxylic acid cycle, is highly expressed in PNF. The present study aimed to explore the role of SUCLG1 in function and metabolism of PNF cells. SUCLG1 expression was verified using western blotting and immunofluorescence. After inducing SUCLG1 knockdown and overexpression, functional changes in PNF cells were assessed, as well as effects of SUCLG1 on cell respiration and glucose metabolism. Quantitative PCR, WB, electron microscopy and Flow cytometry demonstrated that SUCLG1 enhanced mitochondrial quality and promoted mitochondrial fusion, thereby driving proliferation and migration of tumor cells, inhibiting apoptosis and altering the cell cycle. A Seahorse assay showed that elevated SUCLG1 expression enhanced cell aerobic respiration without affecting the glycolytic process. This suggests that SUCLG1 upregulation in PNF does not trigger the Warburg effect associated with malignant tumors. This study also demonstrated the positive regulation of cellular function by promoting the expression level of the gene when SUCLG1 expression was elevated. In conclusion, SUCLG1 altered the mechanism of mitochondrial quality control to enhance cell aerobic respiration, thereby driving the pathogenesis of PNF. Thus, SUCLG1 can serve as a potential target in future therapeutic strategies.
Emerging roles of angiopoietin‑like 4 in human tumors (Review).
Liu R, Fu M, Chen P … +6 more , Liu Y, Huang W, Sun X, Zhu P, Wen Z, Cheng Y
Int J Oncol · 2025 Feb · PMID 39704206 · Full text
Angiopoietin‑like 4 (ANGPTL4), a member of the angiopoietin family, plays critical roles in angiogenesis, lipid metabolism and inflammation. It has been demonstrated that ANGPTL4 has significant influence on various dise...
Angiopoietin‑like 4 (ANGPTL4), a member of the angiopoietin family, plays critical roles in angiogenesis, lipid metabolism and inflammation. It has been demonstrated that ANGPTL4 has significant influence on various diseases. Accumulating evidence has highlighted the impacts of ANGPTL4 on human malignancies. ANGPTL4 is commonly overexpressed in various types of cancer, such as breast, non‑small cell lung, gastric and colorectal cancer. Its upregulation promotes tumor growth, invasion, metastasis and angiogenesis, as well as metabolic reprogramming and resistance to programmed cell death, radiotherapy and chemotherapy. However, ANGPTL4 has also exhibited antitumor effects under certain conditions, indicating its complex roles in tumor biology. The transcriptional regulation of ANGPTL4 is influenced by multiple factors, such as HIF‑1, PPARs, TGF‑β and long non‑coding RNAs. In terms of signaling pathways, STATs, PI3K/AKT and COX-2/PGE2 are important in regulating cellular processes. The present review summarizes the biological functions of ANGPTL4 in tumors and its association with patient prognosis. Furthermore, the key molecular mechanisms and potential reasons for its dual roles in cancer are also discussed. In conclusion, ANGPTL4 is a valuable diagnostic biomarker and a potential therapeutic target for human cancers.
Non‑coding RNA‑mediated epigenetic modification of ferroptosis in non‑small cell lung cancer (Review).
Wang Y, Fleishman JS, Li Y … +5 more , Cao Y, Wei H, Zhang Z, Chen J, Ding M
Int J Oncol · 2025 Jan · PMID 39670309 · Full text
Ferroptosis is a novel form of regulated cell death that plays a key role in inhibiting tumor malignancy. The ferroptosis signalling cascade provides new opportunities for lung cancer therapy. Non‑coding RNA (ncRNA)‑medi...
Ferroptosis is a novel form of regulated cell death that plays a key role in inhibiting tumor malignancy. The ferroptosis signalling cascade provides new opportunities for lung cancer therapy. Non‑coding RNA (ncRNA)‑mediated epigenetic modification can influence the vulnerability of cancer cells to ferroptosis in non‑small‑cell lung cancer (NSCLC). The present review describes the core molecular mechanisms underlying ferroptosis and the role of epigenetic mechanisms in regulating ferroptosis in NSCLC, as well as developments in understanding the ncRNA‑induced mechanisms that affect ferroptosis in NSCLC. The present review aimed to enhance understanding of the epigenetic mechanisms mediated by ncRNAs that modulate ferroptosis in NSCLC, highlighting a novel therapeutic strategy for NSCLC via the ncRNA‑ferroptosis axis.
MicroRNAs and their role in breast cancer metabolism (Review).
Lee WX, Yeo BS, Mahmud R … +3 more , Tan GC, Wahid MIA, Cheah YK
Int J Oncol · 2025 Jan · PMID 39635852 · Full text
Breast cancer (BC) continues to be the leading cause of cancer‑related mortality among women, placing a substantial disease burden on the global female population. MicroRNAs (miRNAs) are members of a large class of non‑c...
Breast cancer (BC) continues to be the leading cause of cancer‑related mortality among women, placing a substantial disease burden on the global female population. MicroRNAs (miRNAs) are members of a large class of non‑coding RNAs capable of regulating gene expression at the post‑transcriptional level. With cases of early‑onset BC on the rise, miRNAs are promising biomarkers and therapeutic targets for early BC detection and treatment. Dysregulated miRNA expression is known to be closely linked to BC development and metastasis in cancer cells via metabolic reprogramming. Normal cellular metabolism is tightly regulated by various complex signaling pathways. Therefore, dysregulation of metabolism due to metabolic reprogramming is considered a hallmark of cancer. The present review delves into the crucial roles that miRNAs serve in disordered cellular metabolism of BC by targeting gene transcripts, key metabolic enzymes and transporter proteins responsible for regulating major cellular metabolism pathways. The future outlook and clinical implications of miRNAs as potential diagnostic, prognostic and therapeutic markers in BC metabolism are also discussed.
Role of vascular endothelium and exosomes in cancer progression and therapy (Review).
Dai Y, Yao Y, He Y … +1 more , Hu X
Int J Oncol · 2025 Jan · PMID 39635838 · Full text
Cancer poses a significant global health challenge and its progression is intricately connected to the interplay among various cell types and molecular pathways. In recent years, research has focused on the roles of vasc...
Cancer poses a significant global health challenge and its progression is intricately connected to the interplay among various cell types and molecular pathways. In recent years, research has focused on the roles of vascular endothelial cells (VECs) and exosomes within the tumor microenvironment. Anomalies in tumor vascular integrity and function create a conducive milieu for cancer cell proliferation. Despite efforts in clinical anti‑angiogenic interventions, the anticipated outcomes remain elusive. VECs have the capability to transition into mesenchymal cells through endothelial‑to‑mesenchymal transition, thereby affecting cancer advancement. Exosomes are minute membrane‑bound vesicles generated by cells, serving as vital extracellular elements that facilitate cell‑to‑cell communication. They participate in modulating the tumor microenvironment, thereby influencing tumor progression, metastasis, drug resistance and angiogenesis. Additionally, exosomes serve as efficient carriers for drug delivery, as well as targeting and suppressing tumor cells. In summary, understanding the intricate and interconnected mechanisms of VECs and exosomes in cancer, encompassing tumor angiogenesis, microenvironment modulation and immune regulation, is crucial. A comprehensive exploration of these mechanisms may provide insight into cancer treatment and prevention and yield novel therapeutic targets.
Anti‑angiogenic effect of ‑derived peptide via aquaporin 3 in non‑small cell lung cancer.
Kim H, Jung SH, Jo S … +3 more , Han JW, Yoon M, Lee JH
Int J Oncol · 2025 Jan · PMID 39611488 · Full text
Developing novel anti‑angiogenic agents with minimal toxicity is notably challenging for cancer therapeutics. The discovery and development of peptides, whether derived from natural sources or synthesized, has potential...
Developing novel anti‑angiogenic agents with minimal toxicity is notably challenging for cancer therapeutics. The discovery and development of peptides, whether derived from natural sources or synthesized, has potential for developing anti‑angiogenic agents characterized by their ability to penetrate cancer cells, high specificity and low toxicity. The present study identified a ‑derived anticancer and anti‑angiogenesis marine‑derived peptide 06 (MP06). A 22‑amino acid peptide was synthesized and conjugated with fluorescein isothiocyanate (FITC‑MP06) for intracellular localization in H1299 non‑small cell lung cancer cells. Regulatory effects of this peptide on the viability, migration and self‑renewal of lung cancer cells was assessed. Furthermore, anti‑angiogenic effect of MP06 was investigated by monitoring vascular tube formation in human umbilical vein endothelial cells and a zebrafish model. Aquaporin (AQP)3, a membrane channel in various tissues, is involved in regulating stemness, epithelial‑mesenchymal transition (EMT) and angiogenesis. MP06 downregulated AQP3 expression. Consistently, AQP3 knockdown by RNA silencing downregulated its gene expression, leading to a decrease in stemness, EMT and angiogenesis properties in H1299 cells. MP06 could thus serve as a novel therapeutic target with anticancer and angiogenesis properties for non‑small cell lung cancer.
MYBBP1A‑mediated IGFBP4 promoter methylation promotes epithelial‑mesenchymal transition and metastasis through activation of NOTCH pathway in liver cancer.
Sun Y, Weng X, Chen W … +10 more , Ge J, Ding B, Ru J, Lei Y, Hu X, Man D, Cheng S, Duan R, Ren J, Yang B
Int J Oncol · 2025 Jan · PMID 39611481 · Full text
Metastatic hepatocellular carcinoma (HCC) seriously threatens patients' prognosis. It was previously suggested that the insulin growth factor binding protein (IGFBP) family could serve as cancer suppressors in the develo...
Metastatic hepatocellular carcinoma (HCC) seriously threatens patients' prognosis. It was previously suggested that the insulin growth factor binding protein (IGFBP) family could serve as cancer suppressors in the development and metastasis of HCC. However, the role of IGFBP4 and its underlying molecular mechanism in HCC metastasis is elusive. In the present study, it was found that IGFBP4 is significantly downregulated in HCC, whose expression is positively correlated with the prognosis of patients with HCC. Overexpression of IGFBP4 restrained migration abilities and cancer metastasis of HCC cells both and . Furthermore, it was found that IGFBP4 represses HCC metastasis by inhibiting epithelial‑mesenchymal transition. Molecular mechanism studies showed that overexpression of IGFBP4 obviously suppresses NOTCH1 signaling in HCC. As for the upstream regulatory mechanism, it was revealed that downregulation of IGFBP4 in HCC was caused by CpG islands' hyper‑methylation‑dependent degradation mediated by MYBBP1A. Inhibition of MYBBP1A limited HCC metastatic ability and silence of IGFBP4 at the same time restored HCC metastatic potentials. Clinical data demonstrated that low expression of IGFBP4 was found in patients with HCC, especially with lymphatic metastasis. High MYBBP1A expression and low IGFBP4 expression in HCC were correlated with poor survival of patients with HCC. Summarily, in the present study, it was revealed that MYBBP1A/IGFBP4/NOTCH1 pathway could play a crucial role in the progression and metastasis of HCC, which stimulates novel therapeutic and diagnostic strategies against metastatic HCC.
[Corrigendum] Anti‑carcinogenic properties of omeprazole against human colon cancer cells and azoxymethane‑induced colonic aberrant crypt foci formation in rats.
Patlolla JMR, Zhang Y, Li Q … +2 more , Steele VE, Rao CV
Int J Oncol · 2025 Jan · PMID 39611473 · Full text
Following the publication of the above article, an interested reader drew to the authors' attention that certain of the in vitro image panels shown in Fig. 3B (featuring the effects of adding five different concentration...
Following the publication of the above article, an interested reader drew to the authors' attention that certain of the in vitro image panels shown in Fig. 3B (featuring the effects of adding five different concentrations of omeprazole on acridine orange/ethidium bromide‑stained HCA‑7 cells) and Fig. 4 (showing western blotting experiments) on p. 173 and 174 respectively contained overlapping data panels, where results that were intended to represent the results of differently performed experiments had apparently been derived from the same original sources. Specifically, the image panels for 0 and 50 µM/ml omeprazole (Fig. 3Ba and Bb), and 100 and 200 µM/ml omeprazole (Fig. 3Bc and Bd), in Fig. 3B were strikingly similar; and the bands shown for p21 and cyclin A in Fig. 4A and B respectively were also similar, albeit each set of protein bands were turned through 180° relative to the other. After having examined their original data, the authors realized that these figures had been inadvertently assembled incorrectly. The revised versions of Figs. 3 (showing the data correctly for the 0, 100 and 300 µM/ml omeprazole experiments) and 4 (with the cyclin A data omitted) are shown on the next page. Note that the edits made to these figures do not affect the overall results and conclusions reported in the paper. The authors are grateful to the Editor of for granting them the opportunity to publish this corrigendum, and all the authors agree with its publication; furthermore, they apologize to the readership of the journal for any inconvenience caused. [International Journal of Oncology 40: 170‑175, 2012; DOI: 10.3892/ijo.2011.1214].
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