Oncol. Rep. [JOURNAL]
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200 papers
Hypoxic CAF studies unveil PTHrP‑vitamin D‑RAS axis as pivotal in the CAF.
Nakajo S, Uemura M, Kusafuka H … +14 more , Osaki M, Kusunoki C, Takiguchi N, Takeda M, Sekido Y, Hata T, Hamabe A, Ogino T, Miyoshi N, Tei M, Kagawa Y, Yamamoto H, Doki Y, Eguchi H
Oncol Rep · 2026 Jun · PMID 41952490 · Full text
Cancer‑associated fibroblasts (CAFs) play critical roles in the tumor microenvironment (TME); however, their characteristics under hypoxic conditions remain incompletely understood. The aim of the present study was to in...
Cancer‑associated fibroblasts (CAFs) play critical roles in the tumor microenvironment (TME); however, their characteristics under hypoxic conditions remain incompletely understood. The aim of the present study was to investigate the properties of hypoxic CAFs and identify their regulatory factors in colorectal cancer (CRC). CAFs cultured under normoxic and hypoxic conditions were analyzed using proliferation assays, co‑culture experiments, shotgun proteomics and single‑cell RNA sequencing. Clinical specimens were evaluated immunohistochemically using the desmoplastic reaction (DR) classification. In addition, the generalizability of the findings was validated by correlation analyses using The Cancer Genome Atlas database. Hypoxic CAFs showed enhanced proliferative capacity, and their conditioned medium promoted migration and chemoresistance in CRC cells. Shotgun proteomics revealed a significant increase in vitamin D‑binding protein in the conditioned media of hypoxic CAFs, while single‑cell RNA sequencing showed enrichment of genes related to bone metabolism and the phosphoinositide 3‑kinase‑AKT signaling pathway. Treatment of normal fibroblasts (NFs) with parathyroid hormone‑related protein (PTHrP) induced CAF‑like phenotypes, whereas treatment of CAFs with vitamin D led to morphological changes toward a NF‑like appearance. In clinical samples, the immature DR subtype, associated with poor prognosis, exhibited increased expression of the hypoxia marker hypoxia‑inducible factor‑1α, periostin and PTHrP, along with a significant association with Kirsten rat sarcoma viral oncogene homolog (KRAS) mutations. Furthermore, a strong positive correlation was observed between the copy numbers of PTHrP and KRAS across multiple cancer types, including CRC. These findings suggest that the PTHrP‑vitamin D‑rat sarcoma oncogene (RAS) axis functions as an important regulatory mechanism in hypoxic CAFs. PTHrP and vitamin D may influence each other's activity, and this axis may contribute to tumor progression within the TME. Therefore, the PTHrP‑vitamin D‑RAS axis could serve as a potential therapeutic target.
[Retracted] miR‑24‑3p regulates bladder cancer cell proliferation, migration, invasion and autophagy by targeting DEDD.
Yu G, Jia Z, Dou Z
Oncol Rep · 2026 Jun · PMID 41952488 · Full text
Following the publication of the above article, a concerned reader drew to the Editor's attention that, regarding the cell migration assay experiments shown in Fig. 3B, the 'miR‑24‑3p inhibitor' panels that had been incl...
Following the publication of the above article, a concerned reader drew to the Editor's attention that, regarding the cell migration assay experiments shown in Fig. 3B, the 'miR‑24‑3p inhibitor' panels that had been included to represent the T24 and HBC cell lines contained an overlapping section of data, such that data which were intended to show the results of different experiments had apparently been derived from the same original source. Upon performing an independent analysis of the data in this paper in the Editorial Office, it subsequently came to light that several of the western blot data featured in Fig. 3E were strikingly similar to data that appeared in five other papers (one of which was received earlier than this paper at with no authors held in common); in addition, cell invasion assay data featured in Fig. 2G were also strikingly similar to data which appeared in a pair of subsequently published papers that too featured no authors in common. Given the issue of data sharing and the fact that certain of the western blot data had been included in an article that was already been submitted for publication to another journal, the Editor of has decided that this paper should be retracted from the Journal on account of a lack of confidence in the presented data. 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. [Oncology Reports 37: 1123‑1131, 2017; DOI: 10.3892/or.2016.5326].
[Expression of Concern] 5‑Azacytidine inhibits the proliferation of bladder cancer cells via reversal of the aberrant hypermethylation of the hepaCAM gene.
Wang X, Chen E, Yang X … +4 more , Wang Y, Quan Z, Wu X, Luo C
Oncol Rep · 2026 Jun · PMID 41930589 · Full text
Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that, regarding the immunohistochemical images shown in Fig. 1A on p. 1377, the 'DNMT3A' and 'DNMT3B' images for...
Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that, regarding the immunohistochemical images shown in Fig. 1A on p. 1377, the 'DNMT3A' and 'DNMT3B' images for the 'BN' row of data contained an overlapping section, such that date which were intended to show the results from differently performed experiments had apparently been derived from the same original source. In addition, upon performing an independent analysis of the data in this paper in the Editorial Office, it came to light that the same data had been included for the Petri dish images in Fig. 3B on p. 1382 for the DMSO experiments with the T24 and EJ cell lines, albeit the EJ image had been rotated through 90°. The authors were contacted by the Editorial Office to offer an explanation for this apparent duplication of data within these figures; however, up to this time, no response from them has been forthcoming. Owing to the fact that the Editorial Office has been made aware of potential issues surrounding the scientific integrity of this paper, we are issuing an Expression of Concern to notify readers of this potential problem while the Editorial Office continues to investigate this matter further. [Oncology Reports 35: 1375‑1384, 2016; DOI: 10.3892/or.2015.4492].
HMGB3: A pivotal orchestrator of therapy resistance and cancer stemness in human malignancies (Review).
Zhang J, Sun Y, Wang L … +4 more , Gu J, Hua Y, Shao J, Feng N
Oncol Rep · 2026 Jun · PMID 41930588 · Full text
High mobility group box 3 (HMGB3) acts as an essential participator in fundamental biological processes, including transcriptional regulation, chromatin remodeling and DNA repair. HMGB3 is highly expressed and functional...
High mobility group box 3 (HMGB3) acts as an essential participator in fundamental biological processes, including transcriptional regulation, chromatin remodeling and DNA repair. HMGB3 is highly expressed and functionally essential during embryonic development, particularly in the hematopoietic and nervous systems, but it is significantly downregulated or silenced in most normal adult tissues. Its aberrant upregulation has been revealed in numerous human malignancies, such as leukemia, as well as breast, bladder, colorectal and gastric cancer, and its expression levels have been established to be closely associated with poor prognosis of specific patients. Accordingly, the present review systematically explores the central roles of HMGB3 in mediating resistance to cancer therapy. This review focuses on its multifaceted mechanisms of maintaining cancer stemness, enhancing DNA damage repair, modulating cell death pathways and remodeling the tumor microenvironment, thereby contributing to the resistance to chemotherapy, radiotherapy, targeted therapy and immunotherapy collectively. HMGB3 can be accepted as a key target in the development of highly promising therapeutic strategies, given its pivotal involvement in multidrug resistance, which may offer novel avenues for overcoming clinical treatment resistance and improving patient outcomes.
[Retracted] Ultrasound‑targeted microbubble destruction‑mediated overexpression of Sirtuin 3 inhibits the progression of ovarian cancer.
Cheng L, Zhang D, Yan W
Oncol Rep · 2026 Jun · PMID 41930579 · Full text
Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that certain of the data showing the results of EdU assay experiments in Fig. 2C on p. 5 were strikingly similar to da...
Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that certain of the data showing the results of EdU assay experiments in Fig. 2C on p. 5 were strikingly similar to data that had either already been submitted for publication, or which were already published, in articles in other journals that were written by different authors at different research institutes (a couple of which have subsequently been retracted). Furthermore, there appeared to be one instance of duplication of western blot data comparing Fig. 1D with Fig. 5A. In view of the fact that the abovementioned data had already been submitted for publication, or were already published, elsewhere before this paper was received at , the Editor 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. [Oncology Reports 46: 220, 2021; DOI: 10.3892/or.2021.8171].
T cell fate regulation in EBV‑associated nasopharyngeal carcinoma (Review).
Zhang L, Ding S, Chen D … +2 more , Cai B, Mu Z
Oncol Rep · 2026 Jun · PMID 41930573 · Full text
Nasopharyngeal carcinoma, a malignancy associated with Epstein‑Barr virus, presents a complex immune editing landscape in which T cell fate determination carries out a central role. T cell metabolic exhaustion, Epstein‑B...
Nasopharyngeal carcinoma, a malignancy associated with Epstein‑Barr virus, presents a complex immune editing landscape in which T cell fate determination carries out a central role. T cell metabolic exhaustion, Epstein‑Barr virus antigen presentation and tertiary lymphoid structure remodeling are important in the context of tumor immune evasion. Although individual mechanisms have been extensively studied, their interplay and collective contribution to immune editing remain incompletely understood. The present review summarizes the current advances in nasopharyngeal carcinoma immune editing, with a focus on the molecular network underlying T cell fate decisions. How these mechanisms can be leveraged to develop novel immunotherapeutic strategies is further discussed. By integrating recent findings, the present review aims to offer new insights into the intricate immune landscape of nasopharyngeal carcinoma and to provide a theoretical basis for improving immunotherapy efficacy.
Role of CHD4 in tumor progression, DNA damage response and treatment resistance (Review).
Li S, Ma Q, Lian K … +2 more , Jiang Z, Ma Y
Oncol Rep · 2026 Jun · PMID 41930570 · Full text
Chromodomain helicase DNA‑binding protein 4 (CHD4) is a core adenosine triphosphate (ATP)‑dependent chromatin‑remodeling factor of the nucleosome‑remodeling and deacetylase (NuRD) complex. It plays a crucial role in chro...
Chromodomain helicase DNA‑binding protein 4 (CHD4) is a core adenosine triphosphate (ATP)‑dependent chromatin‑remodeling factor of the nucleosome‑remodeling and deacetylase (NuRD) complex. It plays a crucial role in chromatin structure regulation, gene expression regulation, and DNA damage response. It has been demonstrated that CHD4 has context‑dependent functions in tumor development and progression. It can influence tumor progression via such mechanisms as regulating tumor‑related signaling pathways, maintaining the silencing of tumor suppressor genes, and promoting metabolic adaptation; it can also exert tumor‑suppressive effects in specific transcriptional regulatory environments. Additionally, during DNA damage response, CHD4 participates in chromatin remodeling at damage sites, in cell cycle recovery, and in repair pathway selection. It is also involved in the development of tumor treatment resistance through mechanisms that include regulation of DNA repair, cell cycle progression, drug efflux, the tumor immune microenvironment, and replication fork stability. It has also been shown that various non‑coding RNAs participate in the functional regulation of CHD4 by modulating its expression, localization, and protein stability. In summary, as a key node connecting chromatin regulation, genome stability, and tumor treatment response, CHD4 holds significant importance in tumor progression and treatment.
ZBTB7A promotes malignant phenotypes in ovarian cancer through transcriptional activation of CRLF1.
Hao X, Chen Y
Oncol Rep · 2026 May · PMID 41891980 · Full text
Ovarian cancer (OV) remains the most lethal gynecological malignancy, owing to late‑stage diagnosis, high metastatic potential and limited therapeutic efficacy. Although the transcription factor zinc finger and BTB domai...
Ovarian cancer (OV) remains the most lethal gynecological malignancy, owing to late‑stage diagnosis, high metastatic potential and limited therapeutic efficacy. Although the transcription factor zinc finger and BTB domain‑containing 7A (ZBTB7A) has been implicated in several types of cancer, its role in OV has not yet been systematically characterized. The present study comprehensively investigated the expression pattern, prognostic relevance, functional role and downstream mechanisms of ZBTB7A in OV progression. Multi‑cohort transcriptomic analyses across independent public datasets revealed consistent upregulation of ZBTB7A in OV tissues, and high expression predicted a significantly poor prognosis. Single‑cell RNA sequencing demonstrated that ZBTB7A‑high tumor cells were enriched in proliferative, migratory and epithelial‑mesenchymal transition‑related programs, accompanied by activation of oncogenic pathways such as Wnt/β‑catenin and Hippo‑YAP. Functional assays using overexpression and RNA interference demonstrated that ZBTB7A enhanced malignant phenotypes, including increased cell proliferation, DNA synthesis, clonogenic survival and migration. Further analyses identified cytokine receptor‑like factor 1 (CRLF1) as a key downstream effector of ZBTB7A. ZBTB7A overexpression elevated CRLF1 transcription, whereas CRLF1 knockdown abrogated ZBTB7A‑induced proliferation and migration, defining a functional ZBTB7A/CRLF1 oncogenic axis. Collectively, these findings establish ZBTB7A as an important transcriptional driver of OV aggressiveness and highlight the ZBTB7A/CRLF1 regulatory pathway as a potential prognostic biomarker and therapeutic target.
[Retracted] Roles of the SNHG7/microRNA‑9‑5p/DPP4 ceRNA network in the growth and I resistance of thyroid carcinoma cells through PI3K/Akt activation.
Chen W, Yu J, Xie R … +4 more , Zhou T, Xiong C, Zhang S, Zhong M
Oncol Rep · 2026 May · PMID 41891970 · Full text
Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that there appeared to be a series of internally duplicated groupings/repeated patternings of cells within various of...
Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that there appeared to be a series of internally duplicated groupings/repeated patternings of cells within various of the panels in the DPP4 row of data panels in Fig. 8B on p. 14 that could not be easily attributed to coincidence. Secondly, some of the data panels shown in the p‑Akt row of data in Fig. 8B, in addition to certain of the data showing the results of EdU assay experiments in Fig. 3B on p. 8, were strikingly similar to data that had either already been submitted for publication, or which were already published, in articles in other journals that were written by different authors at different research institutes (one of which has subsequently been retracted). Furthermore, there appeared to be one instance of duplication of western blot data comparing Fig. 5K with Fig. 7, and also possible discrepancies between the actual sizes and the reported sizes of the tumours in Fig. 8A. In view of the fact that the abovementioned data had already been submitted for publication, or were already published, elsewhere before this paper was received at , in addition to the other problems with the data and apparent anomalies that have been identified with various of the figures, the Editor has decided that this paper should be retracted from the Journal. After contacting the authors, they accepted the decision to retract the paper. The Editor apologizes to the readership for any inconvenience caused. [Oncology Reports 45: 3, 2021; DOI: 10.3892/or.2021.7954].
MS4322 is a selective protein arginine methyltransferase 5 degrader with antitumor effects in cervical cancer cells.
Luo R, Chen J, Chen Z … +3 more , Wang S, Liu T, Xu Y
Oncol Rep · 2026 May · PMID 41891959 · Full text
Drug therapy serves a key role in the treatment of cervical cancer, which is one of the most common types of solid tumor in female patients. Therefore, it is important to seek more effective and less toxic therapies. Pro...
Drug therapy serves a key role in the treatment of cervical cancer, which is one of the most common types of solid tumor in female patients. Therefore, it is important to seek more effective and less toxic therapies. Protein arginine methyltransferase 5 (PRMT5) is a key oncogenic target in cervical cancer, providing a rational basis for the development of targeted therapeutic agents. MS4322 is a highly selective proteolysis targeting chimera degrader specifically targeting PRMT5. Therefore, the present study aimed to investigate the therapeutic potential of MS4322 against cervical cancer and the underlying molecular mechanisms. The effects of MS4322 on human cervical HeLa cells were investigated by Cell Counting Kit‑8, clone formation, wound healing and Transwell assay, flow cytometry, immunofluorescence staining, immunohistochemistry and small interfering RNA assay. PRMT5 expression was upregulated in cervical cancer tissue, and functional analyses confirmed that PRMT5 promoted the proliferation of cervical cancer cells. MS4322 significantly decreased PRMT5 mRNA expression, as well as the proliferation, migration, invasion and clone formation ability of HeLa cells, leading to cell cycle arrest in G0/G1 phase and inducing apoptosis. Mechanistically, MS4322 downregulated the expression of PRMT5, β‑catenin, Wnt‑3a, and c‑myc, while upregulating GSK‑3β, thereby inactivating the Wnt/β‑catenin pathway. These findings indicated that MS4322 exerted anti‑tumor effects via regulating the PRMT5/Wnt/β‑catenin pathway and may serve as a promising candidate agent for cervical cancer treatment.
Andrographis exerts antitumor effects and enhances 5‑FU efficacy via the alteration of ferroptosis‑related genes in esophageal squamous cell carcinoma.
Yoshimura K, Shimura T, Ma R … +17 more , Huang Y, Kitajima T, Yamashita S, Sato Y, Higashi K, Kawamura M, Yasuda H, Koike Y, Okita Y, Yoshiyama S, Kobayashi M, Ohi M, Ohge H, Takahashi S, Goel A, Okugawa Y, Toiyama Y
Oncol Rep · 2026 May · PMID 41860050 · Full text
Preoperative systemic chemotherapy plays a crucial role in enhancing the outcomes of patients with locally advanced esophageal squamous cell carcinoma (ESCC). Andrographis (major bioactive diterpenoid lactone isolated fr...
Preoperative systemic chemotherapy plays a crucial role in enhancing the outcomes of patients with locally advanced esophageal squamous cell carcinoma (ESCC). Andrographis (major bioactive diterpenoid lactone isolated from ; PubChem ID: 5318517), a safe and cost‑effective dietary compound, has demonstrated antitumor effects against various gastrointestinal adenocarcinomas. However, its impact on squamous cell carcinoma remains unclear. The present study explored the antitumor effects of Andrographis and its potential to augment the antitumor efficacy of 5‑fluorouracil (5‑FU). A series of experiments was conducted, including cell proliferation, colony formation and apoptosis assays, using the ESCC cell lines KYSE410 and TE1. Compared with the controls, Andrographis significantly inhibited cell proliferation (P<0.05), suppressed colony formation (P<0.05), induced apoptosis (P<0.05), and upregulated the expression of ferroptosis‑related genes and proteins, such as HMOX1 (P<0.01), GCLC (P<0.05) and GCLM (P<0.001). Notably, even at a sub‑IC dose of 5‑FU, its combination with Andrographis resulted in additive antitumor effects (P<0.05) and further upregulation of ferroptosis‑related gene expression, particularly HMOX1 (P<0.05), compared with either mono‑treatment. The findings of the present study indicate that Andrographis exerts antitumor effects and enhances the efficacy of 5‑FU in ESCC by activating both apoptosis and ferroptosis, suggesting its potential as an adjunctive therapy for ESCC to improve efficacy and reduce 5‑FU dosage and toxicity.
Sphingosine‑1‑phosphate receptor 1 enhances olfactory receptor 51E1‑mediated inhibition of proliferation via Src/JNK signaling in prostate cancer cells.
Kim K, Lee J, Choi C … +3 more , Bae J, Choi HJ, Huh WK
Oncol Rep · 2026 May · PMID 41860044 · Full text
Olfactory receptors (ORs) are ectopically expressed in multiple cancers and can regulate tumor cell behavior, yet their clinical relevance and regulatory mechanisms remain poorly defined. OR51E1 is highly expressed in pr...
Olfactory receptors (ORs) are ectopically expressed in multiple cancers and can regulate tumor cell behavior, yet their clinical relevance and regulatory mechanisms remain poorly defined. OR51E1 is highly expressed in prostate cancer (PC) and suppresses tumor cell proliferation upon activation, but its expression alone does not correlate with patient prognosis, suggesting additional regulatory factors. Using transcriptomic analyses of The Cancer Genome Atlas and Genotype‑Tissue Expression datasets, functional screening of G‑protein‑coupled receptors, and mechanistic studies in PC cells, sphingosine‑1‑phosphate receptor 1 (S1PR1) was identified as a key modulator of OR51E1 function. Activation of OR51E1 by nonanoic acid (NA) or butyric acid reduced PC cell survival in an OR51E1‑dependent manner, and this effect was abolished in OR51E1 knockout cells. S1PR1 enhanced OR51E1‑mediated signaling by increasing its surface expression and amplifying downstream apoptotic responses. Although OR51E1 activation induced cAMP signaling, NA‑induced cytotoxicity was independent of the canonical Gs/olf‑cAMP pathway and instead required Src and JNK activation, which was further potentiated by S1PR1. Clinically, co‑expression of OR51E1 and S1PR1 was significantly associated with improved progression‑free interval in patients with prostate adenocarcinoma, particularly in stage II disease, whereas OR51E1 expression alone showed no prognostic value. Collectively, these findings define a previously unrecognized OR51E1‑S1PR1 signaling axis that suppresses PC cell survival through Src/JNK‑dependent mechanisms and highlight GPCR‑mediated regulation of ectopic olfactory receptors as a determinant of tumor behavior and patient outcome.
Mechanistic insights into the roles of astragalosides and polysaccharides in gynecological and breast cancers (Review).
Liu R, Lin Z, Li Y … +3 more , Ci Y, Guo Z, Xu Z
Oncol Rep · 2026 May · PMID 41860034 · Full text
, a Qi‑tonifying herb widely used in traditional Chinese medicine, has emerged as a promising adjuvant for female‑predominant malignancies, including breast, ovarian and cervical cancers. Its major bioactive constituents...
, a Qi‑tonifying herb widely used in traditional Chinese medicine, has emerged as a promising adjuvant for female‑predominant malignancies, including breast, ovarian and cervical cancers. Its major bioactive constituents, polysaccharides (APS) and astragalosides (AST), exert multitarget antitumor activities and are widely used as complementary agents in clinical oncology. Nevertheless, key mechanistic gaps persist, particularly regarding the crosstalk among the PI3K/Akt/mTOR, Wnt/β‑catenin, JNK/MAPK and TGF‑β/Smad pathways, as well as the subtype‑ and context‑dependent regulation of molecular effectors governing programmed cell death, epithelial‑mesenchymal transition and immune reprogramming. This uncertainty constrains biomarker discovery and the rational design of combination regimens, thereby limiting the predictability of clinical benefit. The present review systematically collates current research on the molecular mechanisms and signaling networks through which APS and AST modulate breast, ovarian and cervical cancer biology. Available data indicate that these compounds suppress tumor initiation and progression by inhibiting proliferation, inducing programmed cell death, attenuating invasion and metastasis, reshaping antitumor immunity and macrophage polarization, and potentiating chemotherapeutic efficacy while mitigating treatment‑related toxicity. Overall, these insights aim to provide a mechanistic rationale for the clinical integration of as an adjuvant therapy in gynecological and breast cancers, to bridge traditional Chinese medicine with contemporary pharmacology, and to support the development of individualized, integrative therapeutic strategies for breast, ovarian and cervical cancers.
[Corrigendum] 3‑Bromopyruvate and sodium citrate target glycolysis, suppress survivin, and induce mitochondrial‑mediated apoptosis in gastric cancer cells and inhibit gastric orthotopic transplantation tumor growth.
Wang TA, Zhang XD, Guo XY … +2 more , Xian SL, Lu YF
Oncol Rep · 2026 May · PMID 41823566 · Full text
Subsequently to the publication of the above paper, an interested reader drew to the Editor's attention that, regarding the transmission electron microscopy experiments shown in Fig. 9 on p. 1295, the two 'sCt' panels on...
Subsequently to the publication of the above paper, an interested reader drew to the Editor's attention that, regarding the transmission electron microscopy experiments shown in Fig. 9 on p. 1295, the two 'sCt' panels on the left in the lower row, and the '5‑Fu' panel the furthest on the right in the top row and the 'sCt' panel second on the right in the lower row, contained overlapping sections of data, albeit these areas were at different sizes and/or in different orientations. The authors were able to re‑examine their original data files, and realized that the '5‑Fu' panel the furthest on the right in the top row had inadverently been selected incorrectly (the two abovementioned 'sCt' panels on the left in the lower row were correctly placed, showing the different fields of view). The revised version of Fig. 9, now featuring the correct data for the '5‑Fu' panel in the top row, is shown below. Note that the error made in assembling this figure did not affect the overall conclusions reported in the paper. The authors are grateful to the Editor of for allowing them the opportunity to publish this Corrigendum, and apologize to the readership for any inconvenience caused. [Oncology Reports 35: 1287‑1296, 2016; DOI: 10.3892/or.2015.4511].
Silencing of SIVA‑1 promotes cisplatin resistance in gastric cancer via the Bcl‑2/BAX‑mediated mitochondria‑dependent apoptosis pathway.
Shi ZY, Ding ZR, Huang YL … +12 more , Lei YR, Huang HB, Qing Y, Deng MR, Lu XM, Dong XD, Xia LJ, Xu S, Zhong XG, Li L, Kong FB, Wang XT
Oncol Rep · 2026 May · PMID 41823560 · Full text
The aim of the present study was to investigate the effects of SIVA‑1 silencing on the drug resistance and biological functions of cisplatin (DDP)‑resistant human gastric cancer cells (AGS/DDP), and to explore the mechan...
The aim of the present study was to investigate the effects of SIVA‑1 silencing on the drug resistance and biological functions of cisplatin (DDP)‑resistant human gastric cancer cells (AGS/DDP), and to explore the mechanism underlying its occurrence. AGS/DDP cells with stable silencing of SIVA‑1 were established by molecular biology techniques. The Cell Counting Kit‑8 assay was used to investigate the effect of SIVA‑1 silencing on drug sensitivity in AGS/DDP cells by measuring the IC of Adriamycin, DDP and vincristine. The findings demonstrated that the suppression of SIVA‑1 in AGS/DDP cells markedly augmented the resistance to DDP. In addition, cell proliferation, cell migration, cell invasion and cell apoptosis were assessed using colony formation, cell scratch, Transwell and cell apoptosis assays, respectively. The results of these assays demonstrated that silencing SIVA‑1 notably increased the proliferation, migration and invasion of AGS/DDP cells, while concurrently inhibiting their apoptosis. Furthermore, the effects of SIVA‑1 silencing on drug‑resistant gastric cancer cells were confirmed using a subcutaneous xenograft model in nude mice. The results demonstrated that silencing SIVA‑1 led to a notable increase in tumor volume, growth rate and weight. The bioinformatics analyses results indicated that SIVA‑1 may have an interactive relationship with Bcl‑2, BAX, X‑linked inhibitor of apoptosis protein (XIAP), MAPK8 and baculoviral inhibitor of apoptosis repeat‑containing 5 (BIRC5), and could participate in the mitochondria‑dependent apoptosis pathway. The results of reverse transcription‑quantitative PCR and western blotting indicated that silencing SIVA‑1 in AGS/DDP cells promoted the expression levels of Bcl‑2, XIAP, MAPK8 and BIRC5, and inhibited the expression levels of BAX. In conclusion, silencing SIVA‑1 has been shown to modify sensitivity to DDP and biological function in drug‑resistant gastric cancer cells, either directly or indirectly. This phenomenon may be associated with the Bcl‑2/BAX‑mediated, mitochondria‑dependent apoptosis pathway.
[Retracted] Erastin sensitizes glioblastoma cells to temozolomide by restraining xCT and cystathionine‑γ‑lyase function.
Chen L, Li X, Liu L … +3 more , Yu B, Xue Y, Liu Y
Oncol Rep · 2026 May · PMID 41823559 · Full text
Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that, in addition to the apparent duplication of a pair of protein blots between Fig. 3B and E on p. 1469, some o...
Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that, in addition to the apparent duplication of a pair of protein blots between Fig. 3B and E on p. 1469, some of the western blot data featured in the same figure were strikingly similar to data that had already been submitted for publication to the journal in a paper written by different authors at different research institutes. Owing to the fact that the abovementioned data had already been submitted for publication prior to the receipt of this article at , the Editor 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. [Oncology Reports 33: 1465-1474, 2015; DOI: 10.3892/or.2015.3712].
Depleting HIF‑1α attenuates the progression of osteosarcoma, but tumorigenicity is sustained through HIF‑independent pathways.
Kunishima A, Shimizu T, Takimoto T … +9 more , Sagara A, Nobusue H, Hasuwa H, Hasegawa S, Tamaoki Y, Miyake H, Fukuchi Y, Saya H, Muto A
Oncol Rep · 2026 May · PMID 41823542 · Full text
Poor survival of patients with osteosarcoma means that novel therapeutic targets are needed. A previously developed osteosarcoma mouse model revealed that HIF‑1 target genes are upregulated under anchorage‑independent gr...
Poor survival of patients with osteosarcoma means that novel therapeutic targets are needed. A previously developed osteosarcoma mouse model revealed that HIF‑1 target genes are upregulated under anchorage‑independent growth conditions. HIF‑1α is highly expressed at the hypoxic invasion front . Knockout of HIF‑1α attenuates cell growth under hypoxic and non‑adherent conditions , as well as growth of primary and metastatic osteosarcoma in C57BL/6 mice, suggesting key roles for HIF‑1α in osteosarcoma progression. However, tumors with a rich vasculature develop in the absence of HIF‑1α. Thus, the HIF‑independent survival pathways on which HIF‑KO clones depend needs to be identified. The present study revealed that expression of glycolysis‑related genes, which are targets of HIF, decreased in HIF‑KO clones, but the sensitivity of each clone to inhibitors varied: Some were less sensitive than HIF wild‑type cells under hypoxic conditions. Compound screening revealed that the pathways upon which KO clones depend for survival differ. Indeed, inhibiting the mitochondrial electron transport chain, PI3K or mTOR further reduced growth of KO clones under hypoxic conditions, although one clone was less sensitive to these treatments and retained high proliferation capacity under hypoxic conditions. This clone was extremely sensitive to inhibition of the mevalonate synthesis pathway, suggesting that this might be the mechanism underlying resistance to HIF‑targeted therapies. Thus, although HIF‑1 is an attractive therapeutic target for osteosarcoma, it is necessary to identify and inhibit heterogenous HIF‑independent pathways upon which individual tumor cells rely.
POLQ promotes tumor progression and immunosuppression via ATM‑P53 signaling in endometrial cancer.
Zhu N, Wang J, Zhang X … +3 more , Tang K, Gong L, Hu Y
Oncol Rep · 2026 May · PMID 41823540 · Full text
Endometrial cancer (EC) is a one of the most prevalent gynecological malignancies worldwide; however, the molecular mechanisms driving its progression remain insufficiently understood. In the present study, DNA polymeras...
Endometrial cancer (EC) is a one of the most prevalent gynecological malignancies worldwide; however, the molecular mechanisms driving its progression remain insufficiently understood. In the present study, DNA polymerase θ (POLQ), which is implicated in multiple types of cancer, was comprehensively investigated in EC using data from The Cancer Genome Atlas and TNMplot datasets, with further validation in an independent patient cohort. POLQ expression was markedly upregulated in EC tissues and was associated with reduced 15‑year overall survival. Increased POLQ levels were also associated with higher Ki67 proliferation indices, distinct patterns of T‑cell infiltration and enhanced programmed death‑ligand 1 (PD‑L1) expression. Gene Set Enrichment Analysis revealed that POLQ expression was associated with pathways involved in cell proliferation, cell cycle regulation and DNA damage repair. Mechanistic studies based on POLQ knockdown in EC cells were conducted using small interfering RNA‑mediated gene silencing, followed by functional assays including cell proliferation assay, flow cytometric cell cycle analysis, apoptosis assay, migration and invasion assays, and western blot analysis to detect the expression of key proteins involved in ATM/P53 signaling and epithelial‑mesenchymal transition (EMT) regulation. These experiments further demonstrated that POLQ may accelerate EC progression via two complementary mechanisms: i) Activation of ataxia‑telangiectasia mutated/P53 signaling to facilitate cell cycle checkpoint bypass; and ii) induction of EMT via cadherin switching. Collectively, these findings established POLQ as a robust prognostic biomarker and a promising therapeutic target in EC.
Unveiling the role of ANGPT2 in esophageal cancer: A prognostic factor and potential oncogene.
Zhai Z, Xue Z, Fang Y … +8 more , Fan Y, Li S, Yu Y, Chen C, Zhang K, Chen D, Tang X, Ling R
Oncol Rep · 2026 May · PMID 41823527 · Full text
Esophageal cancer (ESCA) is defined by high incidence and mortality rates. Emerging evidence implicates angiopoietin‑2 (ANGPT2) as a key mediator in human carcinogenesis; however, its precise functional role and underlyi...
Esophageal cancer (ESCA) is defined by high incidence and mortality rates. Emerging evidence implicates angiopoietin‑2 (ANGPT2) as a key mediator in human carcinogenesis; however, its precise functional role and underlying mechanisms in ESCA remain incompletely elucidated. Clinical samples and The Cancer Genome Atlas, genotype‑tissue expression and Gene Expression Omnibus databases were first used to analyze ANGPT2 expression, clinical relevance and prognostic value, demonstrating it as an independent prognostic factor and potential oncogene in ESCA. In addition, abnormal ANGPT2 expression affected ESCA migration and invasion . Subsequently, through correlation, expression and prognostic analyses, the upstream long‑chain non‑coding RNAs and microRNAs that regulate ANGPT2 were identified. In conclusion, gene set enrichment analysis revealed a connection between ANGPT2 and the immune system, with ANGPT2 level showing a strong positive correlation with tumor microenvironment cell infiltration, immune cell markers, and immune checkpoint expression. Furthermore, ANGPT2 expression was significantly associated with sensitivity to chemotherapeutic drugs. To summarize, overexpression of ANGPT2 in ESCA is associated with an unfavorable prognosis and compromised tumor immunity.
Unveiling the molecular landscape: Long non-coding RNAs in neuroblastoma (Review).
Xia Z, Zhai H, Zheng L … +1 more , Wang C
Oncol Rep · 2026 May · PMID 41823525 · Full text
Neuroblastoma (NB) is a prevalent malignant tumor in pediatric populations, accounting for 10-15% of childhood cancer-related deaths. Standard treatments include surgery, radiotherapy and chemotherapy; however, in recent...
Neuroblastoma (NB) is a prevalent malignant tumor in pediatric populations, accounting for 10-15% of childhood cancer-related deaths. Standard treatments include surgery, radiotherapy and chemotherapy; however, in recent years, immunotherapy and targeted therapies have also demonstrated encouraging outcomes, particularly for high-risk NB cases. Despite these advances, more than one-third of patients either fail to respond to immunotherapy or eventually develop therapeutic resistance, highlighting the need to further explore the molecular mechanisms driving NB and to develop novel therapeutic approaches. Notably, dysregulated long non-coding RNA (lncRNA) expression is closely associated with NB prognosis, early diagnosis and therapeutic responsiveness. The present review systematically summarizes the molecular mechanisms by which lncRNAs contribute to NB development and progression, and provides an updated overview of their emerging clinical applications as diagnostic, prognostic and therapeutic targets. The current study may offer valuable insights into the future development of lncRNA-based precision diagnostic and therapeutic strategies for NB.
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