Cancer Genetics最新文献

{"title":"Dramatic multifocal osteosarcoma treatment response in the setting of POT1 tumor predisposition syndrome","authors":"Stephen Gilene ,&nbsp;Kristen D'Aquila ,&nbsp;Brittany Cooper ,&nbsp;Sara Szabo ,&nbsp;Joseph G. Pressey","doi":"10.1016/j.cancergen.2025.08.008","DOIUrl":"10.1016/j.cancergen.2025.08.008","url":null,"abstract":"<div><div>INTRODUCTION: POT1 tumor predisposition (POT1-TPD) is associated with a spectrum of malignancies due to loss of function mutations in <em>POT1</em> leading to telomere elongation and genomic instability. Osteosarcoma is the most common primary malignant bone tumor and has a poor prognosis when multifocal. CASE PRESENTATION: A 15-year-old male was found to have a primary right distal femur osteosarcoma with multiple additional bony sites of disease. A <em>POT1</em> splice site variant (c.949+1G&gt;C) was identified both somatically and in the germline consistent with POT1-TPD. Despite extensive multifocality, the tumor displayed marked chemosensitivity to standard of care therapy and long-term remission was achieved. DISCUSSION: Evidence suggests that hereditable alterations in telomeric function including <em>POT1</em> are enriched in sarcoma susceptibility. Furthermore, hereditary tumor predisposition syndromes often increase osteosarcoma risk including a recent report of five patients with POT1-TPD. Multifocal osteosarcoma is rare, but a few retrospective cohorts suggest dismal prognosis. This report details an adolescent male with presumed POT1-TPD who developed synchronous multifocal osteosarcoma exquisitely sensitive to chemotherapy which may represent a unique phenotype for the syndrome.</div></div>","PeriodicalId":49225,"journal":{"name":"Cancer Genetics","volume":"298 ","pages":"Pages 39-43"},"PeriodicalIF":2.1,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144933067","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"High YEATS4 expression characterizes MDM2-amplified liposarcoma","authors":"Andrea Mariani ,&nbsp;Mika Sampo ,&nbsp;Harri Sihto ,&nbsp;Tom Böhling ,&nbsp;Omar Youssef","doi":"10.1016/j.cancergen.2025.08.005","DOIUrl":"10.1016/j.cancergen.2025.08.005","url":null,"abstract":"<div><div><em>YEATS4</em> resides within the 12q13–15 chromosomal region, where it is frequently co-amplified with <em>MDM2</em> and <em>CDK4</em> in liposarcomas (LPS). However, its independent role in LPS progression and dedifferentiation remains poorly defined. In this study, <em>YEATS4</em> expression was analyzed in 57 formalin-fixed paraffin-embedded (FFPE) LPS samples using quantitative real-time PCR and compared across histological subtypes. <em>MDM2</em> amplification status was determined by fluorescence in situ hybridization (FISH). The functional relevance of <em>YEATS4</em> was assessed via siRNA-mediated knockdown in two well-differentiated LPS (WDLPS) cell lines, GOT-3 and 93T449. Relative <em>YEATS4</em> mRNA expression was significantly higher in <em>MDM2</em>-positive compared to <em>MDM2</em>-negative tumors (median = 0.413 vs. 0.007; <em>p</em> = 0.008). Using the median <em>YEATS4</em> expression value (0.227) – calculated from WDLPS and DDLPS cases only – as a threshold, high <em>YEATS4</em> expression was observed in 64% of high-grade dedifferentiated LPS (DDLPS), 54% of low-grade DDLPS, and 29% of WDLPS cases (<em>p</em> = 0.302). Functionally, <em>YEATS4</em> silencing significantly reduced cell viability in 93T449 cells at Days 5 (24.1%) and Day 7 (22.1%) compared to control (<em>p</em> &lt; 0.001). In GOT3 cells, a slight reduction was noted at Day 3 (7.6%) which was not sustained. In summary, <em>YEATS4</em> could contribute to LPS progression in a subset of <em>MDM2</em>-amplified tumors, particularly in high-grade DDLPS. Its variable functional impact across models highlights the complexity of the 12q13–15 amplicon and supports further investigation into <em>YEATS4</em> as a potential molecular marker and therapeutic target in LPS.</div></div>","PeriodicalId":49225,"journal":{"name":"Cancer Genetics","volume":"298 ","pages":"Pages 10-15"},"PeriodicalIF":2.1,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144865487","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Galectin-9 promotes colon cancer development by polarizing macrophages toward the M2 phenotype","authors":"Jun Zhang ,&nbsp;Yang Xu ,&nbsp;Xiao Han ,&nbsp;Yan Gao ,&nbsp;Zhanbo Wei ,&nbsp;Xu Sun","doi":"10.1016/j.cancergen.2025.09.006","DOIUrl":"10.1016/j.cancergen.2025.09.006","url":null,"abstract":"<div><div>Galectin-9 plays multiple roles in various tumors and exerts immune regulation within the tumor microenvironment. It is closely associated with tumor prognosis. This study aimed to analyze the expression of galectin-9 in the colon tumor microenvironment. The results indicated that galectin-9 expression is higher in the colon tumor microenvironment compared to adjacent normal tissues. Furthermore, high expression of galectin-9 was related to M2-type macrophages, which promote tumor development by increasing tumor cell viability, migration, and invasion. Notably, high expression of galectin-9 in colon tumor microenvironment contributed to the polarization of M2 cells, marked by high expression of arginase-1, CD163, and IL-10 and low expression of iNOS. When M0 macrophages were treated with galectin-9 and co-cultured with colon cancer cell lines, it resulted in increased cancer cell growth, migration, and invasion by promoting the differentiation of THP-1 monocytes into the M2 macrophages. The specific mechanism by which galectin-9 promotes M2 polarization involves its binding to Tim-3, recruiting PI3K-p85 to the cytoplasmic domain of Tim-3. This interaction further affects the PI3K/Akt signal pathway, leading to M2 polarization.</div></div>","PeriodicalId":49225,"journal":{"name":"Cancer Genetics","volume":"298 ","pages":"Pages 141-150"},"PeriodicalIF":2.1,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145158112","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hi-C analysis of amplification of MYC, PVT1, and CCDC26 on marker chromosomes in the NB-4 cell line","authors":"Tetsuko Kobayashi ,&nbsp;Satsuki Matsushima ,&nbsp;Hiroaki Ohnishi","doi":"10.1016/j.cancergen.2025.09.004","DOIUrl":"10.1016/j.cancergen.2025.09.004","url":null,"abstract":"<div><div><em>MYC</em> proto-oncogene may be amplified ectopically in acute myeloid leukemia (AML) as extrachromosomal DNA (ecDNA) such as double minutes (dmins). However, the mechanism and location of <em>MYC</em> amplification have not been fully elucidated. To characterize the location of <em>MYC</em> and its surrounding structure in NB-4 cells, we conducted this study using <em>in situ</em> high-throughput chromosomal conformation capture (<em>in situ</em> Hi-C). Hi-C analysis was performed in NB-4 cell line. Whole genome sequencing (WGS) and fluorescence <em>in situ</em> hybridization (FISH) were used for confirmation. Hi-C revealed an inversion involving <em>PVT1</em> and <em>CCDC26</em> and amplified segments involving <em>MYC, PVT1</em>, and <em>CCDC26</em> on 8q24.21 region. <em>MYC, PVT1</em>, and <em>CCDC26</em> were found not only on chromosome 8, but also somewhere intranuclear, other than on chromosome 8. Karyotyping revealed only two normal chromosomes 8, and the others were missing or abnormal. FISH revealed the presence of <em>MYC, PVT1</em>, and <em>CCDC26</em> on the two normal chromosomes 8 and multiple marker chromosomes. Our results suggest that the numerical and structural abnormalities of chromosome 8 precede <em>MYC</em> amplification and moving. <em>MYC</em> may have properties that move not only to dmins, but also to other chromosomes such as marker chromosomes for unknown but certain reasons. <em>MYC</em> ectopic amplification is not only a phenomenon in solid tumors, but also a recurrent phenomenon in AML. Furthermore, in a broader sense, ectopic amplification is a form of abnormal oncogenes. We propose Hi-C as a screening method for this phenomenon. We will further verify this phenomenon in various phases of multiple AML cell lines and patient samples.</div></div>","PeriodicalId":49225,"journal":{"name":"Cancer Genetics","volume":"298 ","pages":"Pages 113-121"},"PeriodicalIF":2.1,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145048474","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification of novel gene fusions in high-grade serous ovarian carcinoma: implications for tumorigenesis and targeted therapy","authors":"Katsuhiro Masago ,&nbsp;Eiichi Sasaki ,&nbsp;Yasuko Fujita ,&nbsp;Shiro Fujita ,&nbsp;Yoshitsugu Horio ,&nbsp;Hiroaki Kuroda ,&nbsp;Aiko Ogasawara ,&nbsp;Kenji Tatsuno ,&nbsp;Hiroyuki Aburatani ,&nbsp;Katsutoshi Oda ,&nbsp;Kosei Hasegawa ,&nbsp;Hirokazu Matsushita","doi":"10.1016/j.cancergen.2025.09.012","DOIUrl":"10.1016/j.cancergen.2025.09.012","url":null,"abstract":"<div><h3>Background</h3><div>High-grade serous ovarian carcinoma (HGSOC) accounts for 70% of all ovarian cancer cases and 80% of related deaths. <em>TP53</em> mutations are common; however, other driving genetic factors are not well understood. In this study, we used RNA sequencing to explore the genetic background of HGSOC in patients with unclear profiles.</div></div><div><h3>Methods</h3><div>This study included 80 patients with a pathological diagnosis of HGSOC. RNA sequencing was performed to analyze gene expression and detect fusion.</div></div><div><h3>Results</h3><div>We identified 18 novel potential driver fusion gene candidates, including in-frame and frameshift fusions, in 80 patients with high-grade serous ovarian cancer (HGSOC). Of these, <em>ST7-OT4::MET, STK24::DOCK9, GAB::PAK1, HDAC1::LCK, ESR1::LATS1, ZNF157::CDK16, NEK7::RP11–85M11.2, CAMKK1::R2RX1, HNRNPUL1::AXL, DYRK1A::GART, MAPKAPK2::DYRK3,</em> and <em>FER::GS1421I3.2</em> involved fusion partners harboring protein kinase domains. Notably, <em>TAOK1::PIPOX</em> and <em>PSMD11::NLK</em> were identified in the same case, similar to <em>SH3PXD2A::BMPR1A</em> and <em>EIF3H::CAMK2D</em> in another case. In addition, <em>SLMAP::NTRK3</em> involves <em>NTRK3</em>, a known fusion partner. The remaining fusions, <em>SWAP70::ZNF143, WDR25::YY1</em>, and <em>NR2F6::MYO9B</em>, included partners with DNA-binding domains.</div></div><div><h3>Conclusions</h3><div>This study identified candidate driver fusion genes and suggested new therapeutic targets for HGSOCs.</div></div>","PeriodicalId":49225,"journal":{"name":"Cancer Genetics","volume":"298 ","pages":"Pages 159-168"},"PeriodicalIF":2.1,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145266621","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Current state of diagnostic genetic testing in pediatric sarcoma: Survey and review by the Cancer Genomics Consortium Sarcoma Working Group","authors":"Kathleen M. Schieffer ,&nbsp;Renu Bajaj ,&nbsp;Selene C. Koo ,&nbsp;Josee Lavoie ,&nbsp;Dolores Lopez-Terrada ,&nbsp;Xinyan Lu ,&nbsp;Minjie Luo ,&nbsp;Thuy Phung ,&nbsp;Teresa A. Smolarek ,&nbsp;Maxine Sutcliffe ,&nbsp;Jennelle C. Hodge ,&nbsp;Cancer Genomics Consortium Sarcoma Working Group","doi":"10.1016/j.cancergen.2025.10.106","DOIUrl":"10.1016/j.cancergen.2025.10.106","url":null,"abstract":"<div><div>The genomic landscape of pediatric sarcomas is constantly expanding, and the utilization of integrated cytogenetic and molecular evaluation of these tumors for diagnosis, prognostication, and therapeutic implications continues to evolve. As a result, there are diverse approaches to the clinical practice of genomic testing in pediatric sarcomas. The Cancer Genomics Consortium Sarcoma Working Group conducted a survey to understand the current state of diagnostic genetic testing for pediatric sarcomas and assess the challenges faced in the field. Among 46 respondents across the United States and Canada, most utilized conventional karyotyping (61 %) and/or fluorescence <em>in situ</em> hybridization (87 %). Molecular methodologies, such as chromosomal microarray (30 %), targeted RT-PCR (22 %), gene fusion sequencing panels (35 %), pan-cancer sequencing panels (37 %), exome sequencing (11 %), and genome sequencing (7 %) were less frequently implemented clinically. When asked about challenges in the field of pediatric sarcoma, a scarcity of standard practice testing guidelines was noted most commonly, especially in the setting of limited tissue availability. Systematic evidence reviews and guidelines are needed for pediatric sarcomas with a consideration for multidisciplinary and international collaboration of individuals representing both high- and low-resource settings. As a resource in the interim, three case-based testing workflow scenarios are presented based on working group member experience to illustrate how differing technologies could be applied during evaluation considering diagnostic, prognostic and/or therapeutic needs. Finally, emerging technologies that are being applied to the diagnostic genetic evaluation of pediatric sarcomas are described, which upon implementation, may serve to streamline the work-up and further optimize patient care.</div></div>","PeriodicalId":49225,"journal":{"name":"Cancer Genetics","volume":"298 ","pages":"Pages 242-255"},"PeriodicalIF":2.1,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145460130","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"WDR54 enhances NF-κB signaling to promote progression of hepatocellular carcinoma","authors":"Hengyong Zhai ,&nbsp;Yanping Du ,&nbsp;Hong He ,&nbsp;Xiaozhou Shen ,&nbsp;Duanmin Hu","doi":"10.1016/j.cancergen.2025.11.007","DOIUrl":"10.1016/j.cancergen.2025.11.007","url":null,"abstract":"<div><div>Hepatocellular carcinoma (HCC) is a major health threat worldwide. This study found that WDR54 is overexpressed in liver cancer tissues and is inversely correlated with patient prognosis. Through comprehensive cell biology experiments, we demonstrated that WDR54 plays a pivotal role in promoting the malignant proliferation and metastasis of HCC. Further molecular biology investigations, including transcriptome sequencing, revealed that WDR54 exerts its biological effects by modulating the NF-κB signaling pathway. Specifically, WDR54 interacts with RBBP5 to enhance the transcription of p65, thereby promoting HCC proliferation and metastasis. Additionally, the potential impact of WDR54 on tumor cell metabolism and tumor heterogeneity is explored. The findings of this study deepen our understanding of the molecular pathology of liver cancer and lay a foundation for future clinical applications.</div></div>","PeriodicalId":49225,"journal":{"name":"Cancer Genetics","volume":"298 ","pages":"Pages 302-314"},"PeriodicalIF":2.1,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145568680","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comprehensive analysis of oncogenic determinants across tumor types via multi-omics integration","authors":"Saba Ubaid ,&nbsp;Rashmi Kushwaha ,&nbsp;Mohammad Kashif ,&nbsp;Vivek Singh","doi":"10.1016/j.cancergen.2025.08.010","DOIUrl":"10.1016/j.cancergen.2025.08.010","url":null,"abstract":"<div><div>Cancer is a complex and heterogeneous disease characterized by the accumulation of genetic and epigenetic alterations that drive uncontrolled cellular proliferation and survival. This review provides a comprehensive overview of key cancer driver genes, including oncogenes such as <em>KRAS</em> and <em>PIK3CA</em>, as well as tumor suppressor genes like <em>TP53, PTEN</em>, and <em>CDKN2A</em>, highlighting their molecular mechanisms and roles across various types of cancer. Leveraging insights from large-scale cancer genome initiatives and whole-genome sequencing, we examine the landscape of somatic mutations and their association with hallmark cancer pathways, including cell cycle regulation, apoptosis, metabolic reprogramming, and immune evasion. Multi-omics integration—encompassing genomic, transcriptomic, proteomic, and epigenomic data has enabled the identification of novel driver mutations, functional interactions, and tumor-specific vulnerabilities. We explore bioinformatics platforms, such as IntOGen, that facilitate the detection and prioritization of driver genes and discuss emerging concepts, including synthetic lethality, chromatin remodeling defects, and epigenetic dysregulation, involving genes like <em>ARID1A, KMT2D</em>, and <em>RB1</em>. Furthermore, we review therapeutic strategies targeting these molecular aberrations, including small-molecule inhibitors, pathway-based therapies, and precision oncology approaches guided by biomarkers. This synthesis underscores the importance of integrating multidimensional data to enhance our understanding of cancer biology and refine personalized treatment strategies for improved patient outcomes.</div></div>","PeriodicalId":49225,"journal":{"name":"Cancer Genetics","volume":"298 ","pages":"Pages 44-62"},"PeriodicalIF":2.1,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144996293","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Synergistic dual oncogenic role of CKS2 and ACAT2: Enhanced regulatory coherence and biomarker potential in adrenocortical carcinoma","authors":"Javad Omidi","doi":"10.1016/j.cancergen.2025.10.103","DOIUrl":"10.1016/j.cancergen.2025.10.103","url":null,"abstract":"<div><div>Adrenocortical carcinoma (ACC) is a rare and highly aggressive endocrine malignancy with limited therapeutic options and poor clinical outcomes. To identify molecular biomarkers with diagnostic and prognostic relevance, an integrative ceRNA network analysis was performed using transcriptomic profiles from TCGA-ACC and GTEx adrenal tissues. miR-466, the highest-centrality miRNA in the ceRNA network, was used as the focal regulatory component in this framework. Experimentally validated targets were obtained from miRTarBase and miRDB, refined by TargetScan binding-site specificity and correlation-based filtering, and evaluated for tumor-specific expression. Among these candidates, CKS2 and ACAT2 emerged as consistently and significantly upregulated across therapy subgroups, with expression patterns confirmed across patient-level clinical heterogeneity. Both genes demonstrated markedly elevated expression in ACC relative to normal adrenal tissue and exhibited reinforced transcriptional co-regulation in tumors, suggesting a coordinated regulatory shift. Kaplan–Meier survival analyses indicated that high expression of either gene was associated with reduced overall survival, while a multivariate CoxPH model integrating both markers stratified patients into distinct high- and low-risk groups. Additionally, ROC classification demonstrated strong diagnostic performance for distinguishing tumor from normal tissue (AUC = 0.90 for CKS2, 0.88 for ACAT2, and 0.90 for the combined logistic regression model). Functional annotation revealed that CKS2 regulates cyclin-dependent cell cycle transitions, while ACAT2 participates in lipid and fatty-acid metabolic pathways. Together, these roles support a synergistic oncogenic axis in which proliferative acceleration is metabolically sustained, reinforcing tumor growth. These findings nominate CKS2 and ACAT2 as robust biomarkers and mechanistic drivers with translational relevance in ACC.</div></div>","PeriodicalId":49225,"journal":{"name":"Cancer Genetics","volume":"298 ","pages":"Pages 221-225"},"PeriodicalIF":2.1,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145410648","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RNF121 promotes the proliferation, migration, and invasion of lung cancer cell lines","authors":"Jun Jiang,&nbsp;Xiaoshuai Chen,&nbsp;Xinjie Dong,&nbsp;Yanfang Wang,&nbsp;Jixuan Liu,&nbsp;Ting Liu,&nbsp;Xiaolei Bian,&nbsp;Ming Li,&nbsp;Yafang Liu","doi":"10.1016/j.cancergen.2025.10.002","DOIUrl":"10.1016/j.cancergen.2025.10.002","url":null,"abstract":"<div><h3>Objectives</h3><div>RING finger proteins are a large family of proteins within the human genome that play essential roles in the regulation of physiological processes and have been implicated in cancer progression. However, the relationships among RING Finger Protein 121 (RNF121), E3 ubiquitin ligase, and tumorigenesis have yet to be determined. In this study, we aimed to comprehensively elucidate the functions of <em>RNF121</em> in non-small cell lung cancer (NSCLC).</div></div><div><h3>Methods</h3><div>On the basis of MTT, colony formation, and Transwell assays, we evaluated <em>RNF121</em>-specific functions that were found to be closely associated with clinicopathological features.</div></div><div><h3>Results</h3><div><em>RNF121</em> expression was demonstrated to be closely associated with different diseases. By altering the levels of this protein in the A549 and H1299 cell lines, we discovered that this protein promotes cell proliferation, migration, and invasion.</div></div><div><h3>Conclusion</h3><div>This study is the first to demonstrate that <em>RNF121</em> plays a prominent role in driving NSCLC progression and that its expression is correlated with clinicopathological features. Accordingly, this gene would serve not only as a key prognostic indicator but also as a novel potential therapeutic target for the treatment of NSCLC.</div></div>","PeriodicalId":49225,"journal":{"name":"Cancer Genetics","volume":"298 ","pages":"Pages 193-197"},"PeriodicalIF":2.1,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145304214","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}