Oncology reports最新文献

{"title":"Triple‑negative breast cancer cell‑derived piR‑31115 promotes the proliferation and migration of endothelial cells via METTL3‑mediated m6A modification of YAP1.","authors":"Shan-Mei Du, Na Li, Wen-Jing Xu, Kui Liu","doi":"10.3892/or.2025.8867","DOIUrl":"10.3892/or.2025.8867","url":null,"abstract":"<p><p>Triple‑negative breast cancer (TNBC), a highly malignant breast cancer subtype with a pronounced metastatic propensity, forms the focus of the present investigation. MDA‑MB‑231, a prevalently utilized TNBC cell line in cancer research, was employed. In accordance with the tumour angiogenesis theory, cancer cells are capable of instigating angiogenesis and the formation of a novel vascular system within the tumour microenvironment, which subsequently sustains malignant proliferation and metastasis. Consequently, impeding the growth of tumour blood vessels holds substantial significance in suppressing TNBC metastasis. Piwi‑interacting RNAs (piRNAs), a category of endogenous non‑coding RNAs, have been demonstrated to modulate cancer progression. However, studies regarding the role of piRNAs in regulating angiogenesis within cancer cells are relatively scant. In the present study, via cell co‑culture experiments, it was revealed that piR‑31115 (a kind of piRNA) in MDA‑MB‑231 cells notably enhanced the recruitment of a human microvascular endothelial cell line (HMEC‑1). Moreover, the conditioned medium (CM, which was obtained from MDA‑MB‑231 cells via a specific culturing methodology and was employed for the subsequent treatment of HMEC‑1 cells to explore its impacts on the biological behaviors such as the proliferation and migration of HMEC‑1 cells) derived from MDA‑MB‑231 cells with upregulated piR‑31115 expression stimulated the proliferation and migration of HMEC‑1 cells. These findings suggest that piR‑31115 in MDA‑MB‑231 cells may play a pivotal role in modulating tumour angiogenesis. Further studies disclosed that the CM from MDA‑MB‑231 cells augmented the N6‑methyladenosine (m6A) RNA modification level via METTL3 in HMEC‑1 cells. Transcriptome sequencing revealed that METTL3 functions as an m6A writer protein for Yes‑associated protein 1 (YAP1), which exerts a positive influence on promoting the proliferation and migration of HMEC‑1 cells. Concurrently, the IGF2BP plays a crucial role in stabilizing YAP1 protein expression. Collectively, the present findings identified a signalling pathway through which MDA‑MB‑231 cells induce HMEC‑1 cell proliferation and migration by regulating m6A RNA methylation.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"53 3","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11755246/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143009124","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] Inhibition of neddylation modification by MLN4924 sensitizes hepatocellular carcinoma cells to sorafenib.","authors":"Zelong Yang, Jie Zhang, Xiaotong Lin, Di Wu, Guixi Li, Chunlian Zhong, Lei Fang, Peng Jiang, Liangyu Yin, Leida Zhang, Ping Bie, Chuan-Ming Xie","doi":"10.3892/or.2025.8866","DOIUrl":"10.3892/or.2025.8866","url":null,"abstract":"<p><p>Following the publication of the above article, the authors noticed that they had inadvertently included a duplication of the same data in Fig. 3C, portraying colony formation experiments, where the results from differently performed experiments were intended to have been shown, and requested that a corrigendum be published to present the data in this figure accurately. Having investigated this matter in the Editorial Office, however, additional panels of overlapping data were identified, comparing between Figs. 2 and 3; moreover, a pair of overlapping data panels were also identified examining the Transwell migration assay data in Fig. 5A. The Editor of <i>Oncology Reports</i> has considered the authors' request to publish a corrigendum, but has decided to decline this request on account of the additional errors that have been identified; rather, the article is to be be retracted from the Journal on the basis of an overall lack of confidence in the presented data. Upon receiving this decision from the Editor, the authors did not provide a satisfactory reply. The Editor apologizes to the readership of the Journal for any inconvenience caused.  [Oncology Reports 41: 3257‑3269, 2019; DOI: 10.3892/or.2019.7098].</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"53 3","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11747261/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143009122","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":"Heteronemin suppresses EGF‑induced proliferation through the PI3K/PD‑L1 signaling pathways in cholangiocarcinoma.","authors":"Yu-Chen S H Yang, Chung-Che Tsai, Yung-Ning Yang, Feng-Cheng Liu, Sheng-Yang Lee, Jen-Chang Yang, Dana R Crawford, Hsien-Chung Chiu, Mei-Chin Lu, Zi-Lin Li, Yi-Chen Chen, Tin-Yi Chu, Jacqueline Whang-Peng, Hung-Yun Lin, Kuan Wang","doi":"10.3892/or.2025.8865","DOIUrl":"10.3892/or.2025.8865","url":null,"abstract":"<p><p>Epidermal growth factor (EGF) binds with its surface receptor to stimulate gene expression and cancer cell proliferation. EGF stimulates cancer cell growth via phosphoinositide 3‑kinase (PI3K) and programmed cell death ligand 1 (PD‑L1) pathways. As an integrin αvβ3 antagonist, heteronemin exhibits potent cytotoxic effects against cancer cells. It inhibits critical signal transduction pathways promoted by the EGF. In the current study, EGF‑induced signal activation and proliferative effects were investigated in cholangiocarcinoma cells and its molecular targets using qPCR and western blotting analyses. In addition, cell viability assays were performed to assess the growth effects of EGF and heteronemin. Heteronemin reversed the effects of EGF and was further enhanced by blockage of PI3K's activity. In summary, EGF stimulates cholangiocarcinoma cell growth. On the other hand, heteronemin inhibited PI3K activation and PD‑L1 expression to reverse the stimulative effects of EGF‑induced gene expression and proliferation in cholangiocarcinoma cells.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"53 3","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142952657","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":"[Retracted] Inhibition of 5‑lipoxygenase triggers apoptosis in pancreatic cancer cells.","authors":"Guo-Xiong Zhou, Xiao-Ling Ding, Sheng-Bao Wu, Hai-Feng Zhang, Wei Cao, Li-Shuai Qu, Hong Zhang","doi":"10.3892/or.2024.8853","DOIUrl":"10.3892/or.2024.8853","url":null,"abstract":"<p><p>Following the publication of the above paper, a concerned reader drew to the Editor's attention that Fig. 3 on p. 664, showing TUNEL assay data relating to apoptosis of the cell line under investigation in this paper, contained apparent anomalies, including repeated patternings of certain cells both within and between the data panels, such that it would have been difficult to have attributed these anomalies to coincidence. After having conducted an independent investigation in the Editorial Office, the Editor of <i>Oncology Reports</i> has determined that the above paper should be retracted from the Journal on account of a lack of confidence concerning the originality and the authenticity of the 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 regrets any inconvenience that has been caused to the readership of the Journal. [Oncology Reports 33: 661‑668, 2015; DOI: 10.3892/or.2014.3650].</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"53 2","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11652959/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142818627","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":"Regulation of pancreatic cancer cells by suppressing KIN17 through the PI3K/AKT/mTOR signaling pathway.","authors":"Qiuyan Li, Yuxia Yang, Xiaocong Lin, Lok Ting Chu, Helian Chen, Linsong Chen, Jinjing Tang, Tao Zeng","doi":"10.3892/or.2025.8864","DOIUrl":"10.3892/or.2025.8864","url":null,"abstract":"<p><p>Pancreatic cancer is an aggressive tumor, which is often associated with a poor clinical prognosis and resistance to conventional chemotherapy. Therefore, there is a need to identify new therapeutic markers for pancreatic cancer. Although KIN17 is a highly expressed DNA‑ and RNA‑binding protein in a number of types of human cancer, its role in pancreatic cancer development, especially in relation to progression, is currently unknown. The present study verified the upregulation of KIN17 in pancreatic cancer using The Cancer Genome Atlas and Gene Expression Omnibus databases (GSE15471, GSE71989 and GSE62165), and identified an association between the PI3K/Akt/mTOR pathway and patient prognosis using publicly available datasets (Gene Expression Profiling Interactive Analysis). Immunohistochemistry was performed to determine the association between KIN17 and the pathological features of clinical pancreatic cancer samples. Furthermore, knockdown of KIN17 was shown to inhibit the migration and invasion of pancreatic cancer cells, and to reverse epithelial‑mesenchymal transition in pancreatic cancer cells through downregulation of Vimentin and N‑cadherin, and upregulation of E‑cadherin. Through various cellular experiments, the role of KIIN17 was explored in PI3K/AKT/mTOR activity. KIN17 inhibition was shown to suppress the migration and invasion of pancreatic cancer cells through PI3K/AKT/mTOR‑mediated autophagy. Furthermore, combined with mTOR inhibition, dual inhibition could enhance autophagy, leading to anti‑migratory and anti‑invasion effects in pancreatic cancer. In conclusion, the present study indicated that KIN17 may have a role in carcinogenesis and could serve as a prognostic biomarker of pancreatic cancer, owing to its high expression. In addition, KIN17 may be considered a potential therapeutic target with its knockdown having an inhibitory effect on pancreatic cancer.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"53 2","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11736091/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142952637","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":"Regulation of the β‑catenin/LEF‑1 pathway by the siRNA knockdown of RUVBL1 expression inhibits breast cancer cell proliferation, migration and invasion.","authors":"Xin Zhang, Dingyuan Cui, Wei Sun, Guangfei Yang, Wen Wang, Chengrong Mi","doi":"10.3892/or.2024.8855","DOIUrl":"10.3892/or.2024.8855","url":null,"abstract":"<p><p>RUVBL1 is a protein characterized by its DNA‑dependent ATPase activity and DNA deconjugating enzyme function. It is a member of the ATPase (AAA+) protein family associated with various cellular processes. Available research confirms that the expression of RUVBL1 is upregulated in breast cancer (BRCA) cell lines; however, the mechanisms underlying its functional role in BRCA remain unclear. The β‑catenin/lymphoid enhancer factor‑1 (LEF‑1) pathway plays a crucial role in the occurrence and development of BRCA. The aim of the present study was to investigate whether RUVBL1 regulates the proliferation, migration and invasion of BRCA cells by participating in the β‑catenin/LEF‑1 signaling pathway. Reverse transcription‑quantitative PCR (RT‑qPCR) and western blot analysis were employed to compare the RUVBL1 expression levels between normal mammary epithelial cells (MCF‑10a) and BRCA cell lines (MDA‑MB‑231 and MCF‑7). Scratch, Cell Counting Kit‑8 and Transwell assays were utilized to assess the effects of RUVBL1 knockdown on the proliferation, migration and invasion of BRCA cells. Following the downregulation of RUVBL1 expression <i>in vitro</i>, western blot analysis and RT‑qPCR were conducted to investigate its role in regulating the β‑catenin/LEF‑1 pathway. The aforementioned experiments proved that the knockdown of RUVBL1 expression inhibited BRCA cell proliferative, migratory and invasive capabilities, modulating the β‑catenin/LEF‑1 pathway. Collectively, the findings of the present study provide preliminarily confirmation that RUVBL1 participates in the molecular mechanisms of the β‑catenin signaling pathway, which may provide a novel target for BRCA treatment.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"53 2","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11667213/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142818804","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":"Impact of miRNAs involved in the STAT3 signaling pathway on esophageal cancer (Review).","authors":"Ying Xiong, Yi-Fan Liu, Zhi-Hui Yang, Cong-Gai Huang","doi":"10.3892/or.2024.8860","DOIUrl":"https://doi.org/10.3892/or.2024.8860","url":null,"abstract":"<p><p>Esophageal cancer (ESCA) is a common tumor noted in the digestive tract, which is highly malignant due to unclear early symptoms and poor last‑stage treatment effects; its mortality rate is relatively high. MicroRNA (miR) and signal transducer and activator of transcription 3 (STAT3) are key components of cellular signaling pathways; their interaction forms a complex and intricate information network that controls several types of biological behaviors in the cells. In the tumor cell, these signal transduction pathways are abnormally active, indicating that the STAT3 signaling pathway mediated by miRs is involved in the progression of various cancer types. The present review introduces the biological characteristics of miR and STAT3 and their relationship with ESCA. It summarizes the regulation of ESCA by the miR and STAT3 signaling pathways and analyzes the effects of these pathways on proliferation, apoptosis, invasion, metastasis and immune escape of cancer cells, as well as the impact on patient survival and prognosis. The purpose of the present review is to assess the miR/STAT3 signaling pathway in ESCA, improve the understanding of the pathogenesis of ESCA and facilitate the identification of therapeutic targets for ESCA.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"53 2","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142922482","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":"Hypoxia studies in non‑small cell lung cancer: Pathogenesis and clinical implications (Review).","authors":"Sirui Zhou, Jiazheng Sun, Weijian Zhu, Zhiying Yang, Ping Wang, Yulan Zeng","doi":"10.3892/or.2024.8862","DOIUrl":"10.3892/or.2024.8862","url":null,"abstract":"<p><p>Non‑small cell lung cancer (NSCLC) is one of the most prevalent and lethal types of cancers worldwide and its high incidence and mortality rates pose a significant public health challenge. Despite significant advances in targeted therapy and immunotherapy, the overall prognosis of patients with NSCLC remains poor. Hypoxia is a critical driving factor in tumor progression, influencing the biological behavior of tumor cells through complex molecular mechanisms. The present review systematically examined the role of the hypoxic microenvironment in NSCLC, demonstrating its crucial role in promoting tumor cell growth, invasion and metastasis. Additionally, it has been previously reported that the hypoxic microenvironment enhances tumor cell resistance by activating hypoxia‑inducible factor and regulating exosome secretion. The hypoxic microenvironment also enables tumor cells to adapt to low oxygen and nutrient‑deficient conditions by enhancing metabolic reprogramming, such as through upregulating glycolysis. Further studies have shown that the hypoxic microenvironment facilitates immune escape by modulating tumor‑associated immune cells and suppressing the antitumor response of the immune system. Moreover, the hypoxic microenvironment increases tumor resistance to radiotherapy, chemotherapy and other types of targeted therapy through various pathways, significantly reducing the therapeutic efficacy of these treatments. Therefore, it could be suggested that early detection of cellular hypoxia and targeted therapy based on hypoxia may offer new therapeutic approaches for patients with NSCLC. The present review not only deepened the current understanding of the mechanisms of action and role of the hypoxic microenvironment in NSCLC but also provided a solid theoretical basis for the future development of precision treatments for patients with NSCLC.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"53 2","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11715622/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142922479","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":"Antibody‑drug conjugates in prostate cancer: Emerging strategies to enhance therapeutic index and current clinical landscape (Review).","authors":"Chadanfeng Yang, Limei Wang, Chen Gong, Dihao Lv, Haihao Li, Yinglong Huang, Jiting Li, Wujie Chen, Shi Fu, Zhiyong Tan, Mingxia Ding","doi":"10.3892/or.2024.8854","DOIUrl":"10.3892/or.2024.8854","url":null,"abstract":"<p><p>The global incidence of prostate cancer (PCa) is rising. Localized PCa can be managed through surgical intervention or radiotherapy, but certain patients may experience recurrence or develop metastatic disease following localized treatment. Despite aggressive therapeutic approaches, the majority of metastatic patients with PCa will eventually progress to metastatic castration‑resistant PCa, with limited treatment alternatives and a dismal prognosis. The treatment options for advanced PCa are continuously evolving, yet there remains a demand for further innovative therapeutic approaches. Antibody‑drug conjugates (ADCs) represent a novel class of targeted medications comprising a humanized monoclonal antibody, a linker and a cytotoxic payload. ADCs primarily bind to antigens that are upregulated on the surface of PCa cells but are minimally expressed on normal cells. At present, a variety of targets for ADCs have been identified in the treatment of PCa, encompassing prostate‑specific membrane antigen, STEAP family member 1, trophoblast cell‑surface antigen 2, CD46, B7‑H3, tissue factor and delta‑like protein 3, each with one or more specific ADC that has shown encouraging results in the PCa field. In the present review, the developmental course, composition and mechanism of action of ADCs are explored, with a specific focus on recently published studies and ongoing trials aimed at investigating the efficacy and safety of ADCs in treating PCa. Lastly, ongoing challenges in ADC development and corresponding strategies to combat them are discussed.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"53 2","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142818692","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":"Epigenetic silencing of <i>JAM3</i> promotes laryngeal squamous cell carcinoma development by inhibiting the Hippo pathway.","authors":"Yue Jia, Jiaojiao Liu, Junqi Shi, Chunming Zhang, Xinfang Wang, Liting Zhao, Yichen Lou, Xiaoya Guan, Hui Huangfu","doi":"10.3892/or.2024.8861","DOIUrl":"10.3892/or.2024.8861","url":null,"abstract":"<p><p>Laryngeal squamous cell carcinoma (LSCC), which represents a significant proportion of head and neck squamous cell carcinoma cases, is often diagnosed at advanced stages, underscoring the urgent need for effective biomarkers and therapeutic targets. Junctional adhesion molecule 3 (<i>JAM3</i>) is implicated in various types of cancer; however, its role in LSCC remains unclear. Therefore, the present study aimed to investigate the epigenetic regulation and tumor‑suppressive functions and mechanisms of <i>JAM3</i> in LSCC. Bioinformatics analysis and 5‑Aza‑2'‑deoxycytidine treatment, which restored <i>JAM3</i> expression as confirmed by reverse transcription‑quantitative PCR and western blotting, revealed that aberrant hypermethylation of the <i>JAM3</i> promoter was associated with reduced <i>JAM3</i> expression and poorer clinical outcomes in patients with LSCC. <i>In vitro</i> experiments, including Cell Counting Kit 8, colony formation and Transwell assays, demonstrated that <i>JAM3</i> overexpression inhibited LSCC cell proliferation, migration and invasion. Western blotting and immunofluorescence analysis revealed that the tumor‑suppressive function of JAM3 was mediated through activation of the Hippo pathway. By contrast, both <i>in vitro</i> and <i>in vivo</i> experiments showed that <i>JAM3</i> knockdown enhanced these oncogenic behaviors by inhibiting the Hippo pathway, suggesting its critical tumor‑suppressive role. In conclusion, the results of the present study indicated that <i>JAM3</i> may be epigenetically downregulated and could function as a novel tumor suppressor gene through the Hippo pathway in LSCC, offering insights into developing targeted treatments and diagnostics.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"53 2","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11718434/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142922474","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}