International journal of oncology最新文献_第7页

Multifaceted roles of lactate dehydrogenase in liver cancer (Review). 乳酸脱氢酶在肝癌中的多重作用（综述）。

IF 4.5 3区医学

International journal of oncology Pub Date : 2025-06-01 Epub Date: 2025-05-26 DOI: 10.3892/ijo.2025.5756

Hai Jin, Qian Liu, Jin Li, Siyu Zhao, Biguang Tuo

{"title":"Multifaceted roles of lactate dehydrogenase in liver cancer (Review).","authors":"Hai Jin, Qian Liu, Jin Li, Siyu Zhao, Biguang Tuo","doi":"10.3892/ijo.2025.5756","DOIUrl":"10.3892/ijo.2025.5756","url":null,"abstract":"Hepatocellular carcinoma (HCC) has high morbidity and mortality rates, and metabolic reprogramming of HCC cells supports the proliferation and development of tumor cells. Lactate dehydrogenase (LDH), a key metabolic enzyme, can maintain the rapid proliferative demand of tumor cells by promoting glycolysis and lactate production in HCC cells. In addition, LDH regulates redox homeostasis and influences lipid synthesis and signaling pathways, further promoting tumor invasion and metastasis. In the tumor microenvironment, LDH affects the function of immune cells and stromal cells by regulating the lactate concentration in and promoting the immune escape and angiogenesis of tumor cells. Since elevated levels of LDH are closely associated with tumor load, invasiveness and poor prognosis, LDH also has promising applications in the early diagnosis, treatment and prognostic assessment of HCC. The present study reviewed the roles of LDH in the occurrence, development, diagnosis, prognosis and treatment of HCC and explored its value as an important biomarker and potential therapeutic target, with the aim of providing a comprehensive reference for HCC‑related research and clinical practice.","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"66 6","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12118952/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144142454","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}

引用次数: 0

[Retracted] Notch1 induces epithelial‑mesenchymal transition and the cancer stem cell phenotype in breast cancer cells and STAT3 plays a key role. 【回缩】Notch1在乳腺癌细胞中诱导上皮-间充质转化和肿瘤干细胞表型，STAT3在其中起关键作用。

IF 4.5 3区医学

International journal of oncology Pub Date : 2025-06-01 Epub Date: 2025-05-16 DOI: 10.3892/ijo.2025.5752

Xiaojin Zhang, Xiaoai Zhao, Shan Shao, Xiaoxiao Zuo, Qian Ning, Minna Luo, Shanzhi Gu, Xinhan Zhao

{"title":"[Retracted] Notch1 induces epithelial‑mesenchymal transition and the cancer stem cell phenotype in breast cancer cells and STAT3 plays a key role.","authors":"Xiaojin Zhang, Xiaoai Zhao, Shan Shao, Xiaoxiao Zuo, Qian Ning, Minna Luo, Shanzhi Gu, Xinhan Zhao","doi":"10.3892/ijo.2025.5752","DOIUrl":"10.3892/ijo.2025.5752","url":null,"abstract":"Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that, in Fig. 3A and B on p. 1145 showing the results of cell invasion and migration experiments, four pairs of overlapping data panels were identified, affecting half the panels shown in the figure, such that these data panels, which were intended to show the results of differently performed experiments, had all apparently been derived from the same original source. Owing to the large number of duplications of data that have been identified in this paper, the Editor of International Journal of Oncology has decided that it 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. [International Journal of Oncology 46: 1141‑1148, 2015; DOI: 10.3892/ijo.2014.2809].","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"66 6","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12101175/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144077958","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}

引用次数: 0

Targeting the cuproptosis‑associated gene COL22A1 in glioblastoma using EMD‑1204831 and kaempferol. 使用EMD - 1204831和山奈酚靶向胶质母细胞瘤中铜增生相关基因COL22A1。

IF 4.5 3区医学

International journal of oncology Pub Date : 2025-05-01 Epub Date: 2025-04-17 DOI: 10.3892/ijo.2025.5744

Yi Chen, Ye Zhang, Huilan Yang, Qiang Liu, Rui Sui, Ji Shi, Haiyang Liang, Jia Liu, Huizhe Xu, Haozhe Piao

{"title":"Targeting the cuproptosis‑associated gene COL22A1 in glioblastoma using EMD‑1204831 and kaempferol.","authors":"Yi Chen, Ye Zhang, Huilan Yang, Qiang Liu, Rui Sui, Ji Shi, Haiyang Liang, Jia Liu, Huizhe Xu, Haozhe Piao","doi":"10.3892/ijo.2025.5744","DOIUrl":"https://doi.org/10.3892/ijo.2025.5744","url":null,"abstract":"Glioblastoma (GBM) is a disease with high morbidity and poor prognosis. The combination of traditional Chinese and Western medicine and cuproptosis are known to serve important roles in the treatment of GBM. However, targeting cuproptosis to treat GBM by combining traditional Chinese and Western medicine has not been extensively investigated. Therefore, the present study focused on the diagnosis and treatment of GBM based on cuproptosis. Through a bioinformatics approach, a cuproptosis‑related prognostic model was first constructed. Next, this prognostic model was found to be closely related to immune infiltration, DNA mutation and DNA methylation through multi‑omics analysis. The present study indicated the cell clusters in GBM tissues and the risk scores in each cluster based on single‑cell sequencing data derived from Gene Expression Omnibus. Notably, by screening the CellMiner database, EMD‑1204831 was found to exhibit a high correlation with the risk score. Next, through network pharmacology and molecular docking analysis, the risk score‑related gene collagen type XXII α1 chain (COL22A1) was identified as the target of kaempferol, which is the active component of Ginseng. Notably, kaempferol could decrease the proliferation of GBM cells by inhibiting COL22A1 expression in cell experiments. Finally, kaempferol and EMD‑1204831 had an obvious inhibitory effect on the growth of GBM and sensitized GBM to cuproptosis inducers via COL22A1 in cell and animal experiments. Overall, the present study revealed a cuproptosis‑related combined regimen for GBM.","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"66 5","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12068844/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143987694","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}

引用次数: 0

[Retracted] Promoter methylation of RASSF1A modulates the effect of the microtubule‑targeting agent docetaxel in breast cancer. RASSF1A启动子甲基化调节微管靶向药物多西他赛在乳腺癌中的作用。

IF 4.5 3区医学

International journal of oncology Pub Date : 2025-05-01 Epub Date: 2025-04-17 DOI: 10.3892/ijo.2025.5745

Eun Young Gil, Uk Hyun Jo, Hoiseon Jeong, Young Mi Whang, Ok Hee Woo, Kyu Ran Cho, Jae Hong Seo, Aeree Kim, Eun Sook Lee, Insong Koh, Yeul Hong Kim, Kyong Hwa Park

{"title":"[Retracted] Promoter methylation of RASSF1A modulates the effect of the microtubule‑targeting agent docetaxel in breast cancer.","authors":"Eun Young Gil, Uk Hyun Jo, Hoiseon Jeong, Young Mi Whang, Ok Hee Woo, Kyu Ran Cho, Jae Hong Seo, Aeree Kim, Eun Sook Lee, Insong Koh, Yeul Hong Kim, Kyong Hwa Park","doi":"10.3892/ijo.2025.5745","DOIUrl":"https://doi.org/10.3892/ijo.2025.5745","url":null,"abstract":"Following the publication of this paper, and a corrigendum that was subsequently published to take account of anomalies that were identified with the assembly of western blot data in Fig. 5B (doi: 10.3892/ijo.2017.3900), a concerned reader drew to the Editor's attention that, regrettably, there remained possible issues with the duplication of data in the revised version of Fig. 5 provided by the authors in the Corrigendum; in addition, potential anomalies were also noted with the western blot assay data in the originally published versions of Fig. 2A and B. After having performed an independent review of the data in these figures in the Editorial Office, the concerns of the reader were found to be validated. Therefore, the Editor of International Journal of Oncology has decided that this paper should now 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. [International Journal of Oncology 41: 611‑620, 2012; DOI: 10.3892/ijo.2012.1470].","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"66 5","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12068852/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143995510","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}

引用次数: 0

[Retracted] lncRNA PLAC2 activated by H3K27 acetylation promotes cell proliferation and invasion via the activation of Wnt/β‑catenin pathway in oral squamous cell carcinoma. 【撤回】H3K27乙酰化激活的lncRNA PLAC2在口腔鳞癌中通过激活Wnt/β - catenin通路促进细胞增殖和侵袭。

IF 4.5 3区医学

International journal of oncology Pub Date : 2025-05-01 Epub Date: 2025-04-04 DOI: 10.3892/ijo.2025.5743

Fubo Chen, Shengcai Qi, Xu Zhang, Jinjin Wu, Xi Yang, Raorao Wang

引用次数: 0

Role of the Wnt signaling pathway in the complex microenvironment of breast cancer and prospects for therapeutic potential (Review). Wnt信号通路在乳腺癌复杂微环境中的作用及其治疗潜力的展望（综述）。

IF 4.5 3区医学

International journal of oncology Pub Date : 2025-05-01 Epub Date: 2025-03-27 DOI: 10.3892/ijo.2025.5742

Meng Xuan Sun, Han Ci Zhu, Yang Yu, Yan Yao, Hua Yao Li, Fu Bin Feng, Qing Yang Wang, Rui Juan Liu, Chang Gang Sun

{"title":"Role of the Wnt signaling pathway in the complex microenvironment of breast cancer and prospects for therapeutic potential (Review).","authors":"Meng Xuan Sun, Han Ci Zhu, Yang Yu, Yan Yao, Hua Yao Li, Fu Bin Feng, Qing Yang Wang, Rui Juan Liu, Chang Gang Sun","doi":"10.3892/ijo.2025.5742","DOIUrl":"10.3892/ijo.2025.5742","url":null,"abstract":"The focus on breast cancer treatment has shifted from the cytotoxic effects of single drugs on tumor cells to multidimensional multi‑pathway synergistic intervention strategies targeting the tumor microenvironment (TME). The activation of the Wnt signaling pathway in the TME of breast cancer cells serves a key regulatory role in tissue homeostasis and is a key driver of the carcinogenic process. Modulating the crosstalk between the Wnt pathway and TME of breast cancer is key for understanding the biological behavior of breast cancer and advancing the development of novel antitumor drugs. The present review aimed to summarize the complex mechanisms of the Wnt signaling pathway in the breast cancer TME, interactions between the Wnt signaling pathway and components of the breast cancer TME and breast cancer‑associated genes, as well as the interactions between the Wnt signaling pathway and other signaling cascades at the molecular level. Furthermore, the present review aimed to highlight the unique advantages of the Wnt signaling pathway in the macro‑regulation of the TME and the current therapeutic strategies targeting the Wnt signaling pathway, their potential clinical value and future research directions in breast cancer treatment.","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"66 5","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12068849/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143719309","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}

引用次数: 0

Mechanism of SMYD2 promoting stemness maintenance of bladder cancer stem cells by regulating PYCR1 expression and PINK1/Parkin mitophagy pathway. SMYD2通过调节PYCR1表达和PINK1/Parkin有丝分裂通路促进膀胱癌干细胞干性维持的机制

IF 4.5 3区医学

International journal of oncology Pub Date : 2025-05-01 Epub Date: 2025-05-09 DOI: 10.3892/ijo.2025.5747

Junjie Chen, Shuai Xiao, Xieyu Yan, Yongbao Wei, Wei Song

{"title":"Mechanism of SMYD2 promoting stemness maintenance of bladder cancer stem cells by regulating PYCR1 expression and PINK1/Parkin mitophagy pathway.","authors":"Junjie Chen, Shuai Xiao, Xieyu Yan, Yongbao Wei, Wei Song","doi":"10.3892/ijo.2025.5747","DOIUrl":"https://doi.org/10.3892/ijo.2025.5747","url":null,"abstract":"SET and MYND domain‑containing protein 2 (SMYD2), an identified protein‑lysine methyltransferase, is key for bladder cancer (BC) progression. The tumor‑formation capacity and metastatic potential of bladder cancer stem cells (BCSCs) are due to their stemness characteristics. The present study explores the mechanism of SMYD2 in promoting BCSC stemness maintenance by pyrroline‑5‑carboxylate reductase 1 (PYCR1). BC cells were treated with PYCR1, SMYD2 and putative kinase 1 (PINK1) small interfering (si)RNA, pcDNA3.1‑PYCR1 and pcDNA3.1‑SMYD2. Mito‑Tracker Green and light chain‑3B (LC3B) expression, in vitro colony formation ability and tumor stemness were assessed, as well as histone H3 lysine 4 trimethylation (H3K4me3) enrichment and PYCR1, SMYD2, H3K4me3, LC3B II/I, p62, PINK1, Parkin, Nanog and SRY‑box transcription factor 2 (Sox2) expression. A nude mouse xenograft model was used for in vivo verification. PYCR1 mRNA and protein expression were elevated in BCSCs. Following PYCR1 or SMYD2 siRNA treatment, PYCR1, SMYD2 and CD44+CD33+ expression, cancer cell colony formation, number of tumor spheres and Nanog and Sox2 expression were decreased, but pcDNA3.1‑PYCR1 or pcDNA3.1‑SMYD2 transfection enhanced BCSC stemness maintenance. SMYD2 was associated with PYCR1 expression. SMYD2 upregulated PYCR1 expression through H3K4me3, subsequently activating the PINK1/Parkin mitophagy pathway, which supports maintenance of BCSC stemness.","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"66 5","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12068851/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143989245","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}

引用次数: 0

SLC4A7 suppresses lung adenocarcinoma oncogenesis by reducing lactate transport and protein lactylation. SLC4A7 通过减少乳酸转运和蛋白质乳化抑制肺腺癌的癌变。

IF 4.5 3区医学

International journal of oncology Pub Date : 2025-05-01 Epub Date: 2025-03-14 DOI: 10.3892/ijo.2025.5739

Haojie Yan, Qian He, Yubiao Gao, Xiaomei He, Haitao Luo, Lijuan Shao, Jun Dong, Furong Li

{"title":"SLC4A7 suppresses lung adenocarcinoma oncogenesis by reducing lactate transport and protein lactylation.","authors":"Haojie Yan, Qian He, Yubiao Gao, Xiaomei He, Haitao Luo, Lijuan Shao, Jun Dong, Furong Li","doi":"10.3892/ijo.2025.5739","DOIUrl":"10.3892/ijo.2025.5739","url":null,"abstract":"Lactate and protein lactylation serve a key role in tumor pathogenesis. Solute carrier 4A7 (SLC4A7), a key transporter, participates in cellular acid homeostasis. However, its impact on lactate transport and protein lactylation in solid tumors, particularly lung adenocarcinoma (LUAD), remains largely unexplored. In the present study, lactylome analysis, Transwell and wound healing assay, animal experiments were conducted to validate functional regulation mediated by SLC4A7 in LUAD. SLC4A7 inhibited tumor progression, including metastasis, invasion and proliferation. Mechanistically, SLC4A7 decreased both intracellular and extracellular lactate accumulation and inhibited overall protein lactylation, as confirmed by lactylome analysis. Analyzing the lactylome revealed that SLC4A7 suppressed lysine lactylation of numerous genes like HSP90AA1 and pathways such as focal adhesion associated with carcinogenesis. Additionally, low expression levels of SLC4A7 in LUAD cancer stem cells were validated using tumor tissue samples from patients with LUAD. Moreover, the inhibitory role of SLC4A7 in regulating tumor stemness was verified. Collectively, the present results uncovered the inhibitory effect exerted by SLC4A7 on tumor progression via its regulation of lactate transport, protein lactylation and stemness properties. Targeting SLC4A7 may hold promise as a novel therapeutic strategy for LUAD.","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"66 5","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12002671/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143623734","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}

引用次数: 0

[Retracted] Role of the EZH2/miR‑200 axis in STAT3‑mediated OSCC invasion. EZH2/miR - 200轴在STAT3介导的OSCC侵袭中的作用。

IF 4.5 3区医学

International journal of oncology Pub Date : 2025-05-01 Epub Date: 2025-03-21 DOI: 10.3892/ijo.2025.5740

Yu Wang, Wenyu Guo, Zhaoqing Li, Yansheng Wu, Chao Jing, Yu Ren, Minghui Zhao, Lingping Kong, Chao Zhang, Jiabin Dong, Yu Shuang, Shanshan Sun, Jinliang Chen, Chuanqiang Wu, Yu Qiao, Xin Qu, Xudong Wang, Lun Zhang, Rui Jin, Xuan Zhou

{"title":"[Retracted] Role of the EZH2/miR‑200 axis in STAT3‑mediated OSCC invasion.","authors":"Yu Wang, Wenyu Guo, Zhaoqing Li, Yansheng Wu, Chao Jing, Yu Ren, Minghui Zhao, Lingping Kong, Chao Zhang, Jiabin Dong, Yu Shuang, Shanshan Sun, Jinliang Chen, Chuanqiang Wu, Yu Qiao, Xin Qu, Xudong Wang, Lun Zhang, Rui Jin, Xuan Zhou","doi":"10.3892/ijo.2025.5740","DOIUrl":"10.3892/ijo.2025.5740","url":null,"abstract":"Following the publication of the above paper, and a corrigendum that has already been published (doi.org/10.3892/ijo.2023.5528) to attend to errors that were made in the assembly of Figs. 2 and 8, it was drawn to the Editor's attention by a concerned reader that two pairs of data panels featuring overlapping data existed comparing Figs. 1C and 2D in the above paper with Fig. 2 in a paper published in the journal Molecular Cancer Therapeutics, which was published before the above paper had been submitted, even though this earlier paper did contain many of the same authors. Given that this further issue has come to light, and owing to the number of duplications of data and errors made in assembling figures that have now been identified in this paper, the Editor of International Journal of Oncology has decided that it should be retracted from the Journal on account of a lack of confidence in the originally 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. [International Journal of Oncology 52: 1149‑1164, 2018; DOI: 10.3892/ijo.2018.4293].","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"66 5","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12002670/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143669719","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}

引用次数: 0

Targeting ncRNAs to overcome metabolic reprogramming‑mediated drug resistance in cancer (Review). 靶向ncRNAs克服癌症中代谢重编程介导的耐药（综述）。

IF 4.5 3区医学

International journal of oncology Pub Date : 2025-05-01 Epub Date: 2025-03-21 DOI: 10.3892/ijo.2025.5741

Junxin Li, Yanyu Li, Lin Fu, Huiling Chen, Fei Du, Zhongshu Wang, Yan Zhang, Yu Huang, Jidong Miao, Yi Xiao

{"title":"Targeting ncRNAs to overcome metabolic reprogramming‑mediated drug resistance in cancer (Review).","authors":"Junxin Li, Yanyu Li, Lin Fu, Huiling Chen, Fei Du, Zhongshu Wang, Yan Zhang, Yu Huang, Jidong Miao, Yi Xiao","doi":"10.3892/ijo.2025.5741","DOIUrl":"10.3892/ijo.2025.5741","url":null,"abstract":"The emergence of resistance to antitumor drugs in cancer cells presents a notable obstacle in cancer therapy. Metabolic reprogramming is characterized by enhanced glycolysis, disrupted lipid metabolism, glutamine dependence and mitochondrial dysfunction. In addition to promoting tumor growth and metastasis, metabolic reprogramming mediates drug resistance through diverse molecular mechanisms, offering novel opportunities for therapeutic intervention. Non‑coding RNAs (ncRNAs), a diverse class of RNA molecules that lack protein‑coding function, represent a notable fraction of the human genome. Due to their distinct expression profiles and multifaceted roles in various cancers, ncRNAs have relevance in cancer pathophysiology. ncRNAs orchestrate metabolic abnormalities associated with drug resistance in cancer cells. The present review provides a comprehensive analysis of the mechanisms by which metabolic reprogramming drives drug resistance, with an emphasis on the regulatory roles of ncRNAs in glycolysis, lipid metabolism, mitochondrial dysfunction and glutamine metabolism. Furthermore, the present review aimed to discuss the potential of ncRNAs as biomarkers for predicting chemotherapy responses, as well as emerging strategies to target ncRNAs that modulate metabolism, particularly in the context of combination therapy with anti‑cancer drugs.","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"66 5","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12002672/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143669678","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}

引用次数: 0