Oncology reports最新文献

{"title":"Loperamide reverses 5‑FU resistance in colorectal cancer by activating autophagy.","authors":"Juan Yu, Xiaotong An, Xinyang Qu, Jing Ke, Huiling Rao, Yang Liu, Zhixin Liu, Danwen Liu, Jie Jia, Shan Li","doi":"10.3892/or.2025.8966","DOIUrl":"10.3892/or.2025.8966","url":null,"abstract":"<p><p>5‑Fluorouracil (5‑FU), a cornerstone chemotherapeutic agent used for colorectal cancer therapy, has long been established as a first‑line treatment. However, clinical evidence has suggested that a substantial proportion of patients develop resistance to 5‑FU, notably compromising its therapeutic efficacy. The present study aimed to investigate whether loperamide (LOP) can enhance the sensitivity of colorectal cancer cells to 5‑FU and to elucidate the potential underlying molecular mechanism. First, the IC₅₀ values of LOP were determined in the 5‑FU‑sensitive HCT8 and 5‑FU‑resistant HCT8R colorectal cancer cell lines, using the Cell Counting Kit‑8 assay to evaluate LOP‑induced alterations in 5‑FU sensitivity. The effects of LOP on cell proliferation were subsequently analyzed using 5‑ethynyl‑2'‑deoxyuridine and colony formation assays. Cell migration was assessed through wound healing and Transwell migration assays, and apoptosis was evaluated using flow cytometric analysis with PI/Annexin V staining. Western blot analysis was performed to measure the expression levels of the autophagy‑associated proteins microtubule‑associated protein 1 light chain 3 (LC3) and Beclin, and autophagosome formation following LOP treatment was visualized. The role of autophagy in LOP‑mediated reversal of drug resistance was further examined using autophagy inhibitors. Finally, xenograft experiments in nude mice were performed to investigate the <i>in vivo</i> effects of LOP on the 5‑FU sensitivity of HCT8R cells. Compared with in the parental cell line, HCT8R cells exhibited enhanced migratory capabilities and resistance to 5‑FU. Notably, LOP was revealed to potentiate the sensitivity of HCT8R cells to 5‑FU, as evidenced by reduced rates of cell proliferation, suppressed migratory ability, increased levels of apoptosis, and decreased tumor weight and volume in subcutaneous xenografts in mice. LOP was also shown to induce upregulation of autophagy marker proteins, leading to the accumulation of autophagosomes within the cells. Blocking autophagy with 3‑methyladenine led to a reversal of the inhibitory effect of LOP on HCT8R cell migration. LOP was also shown to enhance the sensitivity of HCT8R cells to 5‑FU by activating cellular autophagy, thereby suppressing resistant cell proliferation and migration, promoting apoptosis and reversing drug resistance. Taken together, these findings provide novel insights into the mechanisms underlying 5‑FU resistance, thereby highlighting potential therapeutic strategies for colorectal cancer.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"54 4","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12340758/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144799688","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Retracted] Twist induces epithelial‑mesenchymal transition in cervical carcinogenesis by regulating the TGF‑β/Smad3 signaling pathway.","authors":"Qiong Fan, Mei-Ting Qiu, Zhu Zhu, Jin-Hua Zhou, Limo Chen, Ye Zhou, Wei Gu, Li-Hua Wang, Zhu-Nan Li, Ying Xu, Wei-Wei Cheng, Dan Wu, Wei Bao","doi":"10.3892/or.2025.8960","DOIUrl":"10.3892/or.2025.8960","url":null,"abstract":"<p><p>Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that, for the Transwell migration and invasion assay experiments shown in Fig. 3C and D on p. 1791, two pairs of the data panels appeared to be overlapping, suggesting that the same data may have been used in this figure to represent data that were intended to show the results from differently performed experiments. Although the authors responded to the original emailed request from the Editorial Office concerning these data and repeated the experiments shown in this figure, upon performing an independent analysis of the original (published) figures in the office, it came to light that Figs. 1 and 4 also contained probable anomalies. In Fig. 1C and D, there were cells/small areas of the images located in the bottom left hand corners of the images that were strikingly similar, to the extent that this would have been difficult to attribute to coincidence. Furthermore, in the case of Fig. 4, the gel slices in Fig. 4B showed evidence of possible cutting‑and‑splicing events. Owing to the fact that these probable anomalies were also identified that could have affected the interpretation of two additional figures in the published article, the Editor of <i>Oncology Reports</i> has decided that this paper should be retracted from the Journal due to 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 satisfactory reply. The Editor apologizes to the readership for any inconvenience caused. [Oncology Reports 34: 1787‑1794, 2015; DOI: 10.3892/or.2015.4143].</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"54 4","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12329635/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144760663","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of miRNA‑214‑3p in cancer (Review).","authors":"Zeshan Chen, Xin Deng, Yuanhong Lu, Ling Lu, Yijue Qin, Haishun Qu, Shaohang Lan","doi":"10.3892/or.2025.8957","DOIUrl":"10.3892/or.2025.8957","url":null,"abstract":"<p><p>microRNA‑214‑3p (miRNA‑214‑3p) can be mapped to the human chromosome 1q24.3 and is ~22 nucleotides in length. It has been garnering considerable attention due to its aberrant expression profile in various different types of cancer and its apparent role in regulating tumor progression. In malignant tumors, miRNA‑214‑3p can serve as a tumor suppressor or oncogene. This can be mediated by mainly inhibiting the expression of target genes by binding to the 3'‑untranslated region of target mRNAs, thereby regulating multiple downstream cellular processes, such as cell proliferation, metastasis, invasion and apoptosis. However, the role of miRNA‑214‑3p in cancer remains unclear. Therefore, in the present review, the role of miRNA‑214‑3p in cancer was summarized, whilst analyzing its potential as a biomarker for cancer diagnosis, prognosis and response to treatment. In addition, the present review evaluates its effects on sensitivity to chemotherapy, targeted therapy and radiotherapy. The current proposed strategies for the systemic delivery of miRNA‑214‑3p in cancer were also discussed.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"54 4","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12340666/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144760667","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Potential therapeutic target in oncology: Protein palmitoylation (Review).","authors":"Shiping Hao, Yongming Mei, Shaolin Chen, Jing Liu, Yao Zhang, Zhengfeng Zhu, Kangjia Zuo","doi":"10.3892/or.2025.8950","DOIUrl":"10.3892/or.2025.8950","url":null,"abstract":"<p><p>Post‑translational modifications (PTMs) of proteins, by altering the structural conformation of precursor polypeptides, play an indispensable role in augmenting the diversity and stability of the proteome. PTMs exert profound influence on various hallmarks of tumor biology, including cellular proliferation, apoptosis, angiogenesis and metastatic dissemination. Accordingly, advancing our understanding of PTMs holds substantial promise for broadening the therapeutic landscape of oncology. Among these modifications, palmitoylation, a reversible lipid‑based PTM, critically modulates protein stability, membrane localization, protein‑protein interactions and signal transduction cascades. Dysregulation of palmitoylation has been increasingly implicated in tumorigenesis, suggesting its aberrant forms as putative targets for therapeutic intervention. The present review delineates the biochemical mechanisms underlying protein palmitoylation and synthesizes current insights into its multifaceted roles in tumor progression, immune modulation and metabolic regulation, thereby offering novel perspectives for the development of targeted cancer therapies.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"54 4","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12308834/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144668063","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Breaking therapeutic barriers in solid tumors: Clinical progress of antibody‑drug conjugate/immune checkpoint inhibitor combinations (Review).","authors":"Yang Zheng, Yangxuan Ding, Longxia Chen, Zengrui Zhang, Ruilin Ding","doi":"10.3892/or.2025.8956","DOIUrl":"10.3892/or.2025.8956","url":null,"abstract":"<p><p>Cancer has become one of the leading causes of death in most countries. While immune checkpoint inhibitors (ICIs) have revolutionized cancer therapeutics by harnessing antitumor immunity, their clinical application is constrained by intrinsic resistance in most patients and limited responsiveness across specific tumor types. Rational combination strategies may enhance therapeutic outcomes. Antibody‑drug conjugates (ADCs) are an optimal therapeutic partner for synergistic combination with ICIs. ADCs enhance ICI efficacy by inducing immunogenic cell death, which activates tumor‑specific immune responses, remodeling the immunosuppressive tumor microenvironment, and amplifying ICI‑mediated immune cell activation. ADC‑ICI combinations have encouraging antitumor activity across multiple types of solid malignancies. The present review systematically evaluates the synergistic potential of ADC and ICI combination in solid tumor management.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"54 4","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144760665","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"O‑GlcNAcylation as an emerging molecular target for cholangiocarcinoma therapy (Review).","authors":"Purin Charoensuksai, Siwanon Jirawatnotai","doi":"10.3892/or.2025.8952","DOIUrl":"10.3892/or.2025.8952","url":null,"abstract":"<p><p>Aberrant O‑GlcNAcylation and the upregulation of O‑GlcNAc transferase (OGT) are key contributors to cancer pathogenesis and progression, driving hyperproliferative states and metastatic phenotypes. Targeting OGT may suppress cancer progression, positioning OGT and O‑GlcNAc signaling as compelling targets in cancer research. Cholangiocarcinoma (CCA), a rare yet highly aggressive malignancy of the bile duct system, represents a clinical challenge, underscored by its rising global mortality, poor survival outcomes and high recurrence rate, despite advances in awareness, diagnostics and therapeutic strategies. Consequently, there is need for novel therapeutic modalities. Hyperactive O‑GlcNAcylation and upregulation of OGT are observed in CCA, therefore, targeting protein O‑GlcNAcylation may have clinical potential. The present review aimed to summarize the impact of O‑GlcNAcylation on CCA and CCA‑relevant hallmarks of cancer including cell proliferation, metastasis, metabolic reprogramming, angiogenesis, programmed cell death and tumor‑associated inflammation. In areas where direct evidence in CCA is limited, insights from other gastrointestinal tract cancers may identify potential mechanistic connections, offering a broader context to guide future investigation. Furthermore, the viability of OGT and O‑GlcNAcylation as therapeutic targets is discussed.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"54 4","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12308815/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144668062","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Retracted] Upregulation of GRIM‑19 suppresses the growth of oral squamous cell carcinoma <i>in vitro</i> and <i>in vivo</i>.","authors":"Minghe Li, Zhihong Li, Chongyang Liang, Chengmin Han, Wei Huang, Fei Sun","doi":"10.3892/or.2025.8955","DOIUrl":"10.3892/or.2025.8955","url":null,"abstract":"<p><p>Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that certain of the western blot data shown in Figs. 1C and 5C on p. 2186 and p. 2188 respectively were strikingly similar to data that had already been published in articles written by different authors at different research institutes, or which had been included in articles that were already under consideration for publication. Upon investigating this matter independently in the Editorial Office, we were able to confirm the reader's concerns. Therefore, due to the fact that the contentious western blot data in the above article had already been published prior to its submission to <i>Oncology Reports</i>, 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 32: 2183‑2190, 2014; DOI: 10.3892/or.2014.3423].</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"54 4","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12308832/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144708397","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Retracted] MicroRNA-152 inhibits tumor cell growth by directly targeting RTKN in hepatocellular carcinoma.","authors":"Jiejing Zhou, Yanjun Zhang, Yuhong Qi, Dequan Yu, Qiuju Shao, Jun Liang","doi":"10.3892/or.2025.8965","DOIUrl":"10.3892/or.2025.8965","url":null,"abstract":"<p><p>Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that, regarding the flow cytometric plots shown in Figs. 2D and 4C, several of the panels appeared to show similar groupings of dots, which would not have been anticipated if these experiments had been performed discretely under different experimental conditions, suggesting a fundamental flaw either in the way in which these experiments were performed, or in how the results were outputted. The Editor of <i>Oncology Reports</i> 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: 1227-1234, 2017; DOI: 10.3892/or.2016.5290].</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"54 4","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12351223/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144799684","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Histone modifications in cervical cancer: Epigenetic mechanisms, functions and clinical implications (Review).","authors":"Xuewei Li, Min Zhou, Jing Yu, Shaohui Yu, Zheng Ruan","doi":"10.3892/or.2025.8964","DOIUrl":"10.3892/or.2025.8964","url":null,"abstract":"<p><p>Cervical cancer (CC) poses a substantial global health challenge and it ranks as the fourth most prevalent malignancy among women worldwide. Management strategies include surgical intervention, radiotherapy, chemotherapy and emerging systemic treatments. Although advancements in immunotherapy and targeted therapies have been achieved, the aggressive metastatic nature of the disease, coupled with immune evasion and drug resistance, continues to limit overall survival rates. Therefore, there remains an urgent need to identify novel treatment modalities and more effective therapeutic agents. As fundamental regulators of epigenetic modifications, histone alterations serve a critical role in controlling gene expression, DNA repair mechanisms and cellular differentiation. These modifications include acetylation, methylation, phosphorylation, ubiquitination, ADP‑ribosylation and glycosylation, as well as the more recently identified lactylation and palmitoylation. By restructuring chromatin and facilitating interactions among histones, DNA and regulatory proteins, these modifications exert a substantial influence on cellular functions. Aberrant histone modifications contribute to tumorigenesis, tumor heterogeneity and resistance to conventional anticancer therapies, making them a key focus of oncological research. In recent years, therapeutic strategies targeting histone modifications have gained increasing attention in the treatment of CC. Among these epigenetic alterations, histone acetylation and deacetylation have been extensively studied, with numerous histone deacetylase inhibitors showing promise in preclinical studies. The present review explores the patterns of histone modifications in CC, emphasizing their molecular roles in tumor progression, metastasis and therapeutic resistance. Additionally, histone modification‑driven therapeutic targets are examined, laying the groundwork for future precision medicine approaches in CC treatment.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"54 4","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12351160/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144799686","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Advances in the chemo‑preventive effects and mechanisms of ursolic acid against lung cancer (Review).","authors":"Zhanyu Lin, Qingze Chen, Zhaoyue Chen, Tianyang Peng, Jinglu Bai, Fengjun Ma","doi":"10.3892/or.2025.8959","DOIUrl":"10.3892/or.2025.8959","url":null,"abstract":"<p><p>Ursolic acid (UA), a natural pentacyclic triterpenoid carboxylic acid, exhibits diverse biological activities and notable antitumor properties. Lung cancer (LC), a leading malignancy of the respiratory system, is predominantly classified into small cell LC and non‑small cell LC. The increasing incidence and mortality rates of LC have spurred considerable interest in the chemo‑preventive potential of UA. Accumulating evidence demonstrates that UA markedly inhibits LC cell proliferation and induces apoptosis. Mechanistically, UA induces cell cycle arrest at the G0/G1 phase, thereby suppressing LC cell invasion, migration and tumor growth. Furthermore, UA has shown synergistic effects when combined with other therapeutic agents, including mitotic kinase inhibitors and multifunctional nanomedicines, effectively overcoming drug resistance in LC cells. These multifaceted mechanisms collectively contribute to the chemo‑preventive efficacy of UA against LC. Consequently, UA represents a promising candidate for LC prevention and therapy. The present review comprehensively summarizes the anticancer effects and molecular mechanisms of UA in LC, offering insights to guide future research and facilitate the development of innovative therapeutic strategies.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"54 4","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12340665/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144760664","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}