Journal of CancerPub Date : 2025-04-22eCollection Date: 2025-01-01DOI: 10.7150/jca.101406
Jun Gu, Zhen-Duo Shi, Kun Pang, Lin Hao, Wei Wang, Cong-Hui Han
{"title":"Retinoic acid metabolism related gene CYP26B1 promotes tumor stemness and tumor microenvironment remodeling in bladder cancer.","authors":"Jun Gu, Zhen-Duo Shi, Kun Pang, Lin Hao, Wei Wang, Cong-Hui Han","doi":"10.7150/jca.101406","DOIUrl":"10.7150/jca.101406","url":null,"abstract":"<p><p><b>Background</b>: The previous studies have shown that the retinoic acid (RA) metabolism is closely related to the cancer stemness, but its role in bladder cancer development has not been fully investigated. <b>Methods</b>: We conducted a comprehensive analysis of mutations, copy number variations and transcriptional changes of RA metabolism related genes in bladder cancer cells. We evaluated the activity of RA metabolism in tumor cells by using single cell transcriptome data and identified differentially expressed genes (DEGs) in cell subsets with high RA-metabolism score. We also investigated and verified the biological function of <i>CYP26B1</i> (one of RA metabolism related genes) <i>in vitro</i>. Additionally, we analyzed and verified the relationship between <i>CYP26B1</i> and tumor immune microenvironment by multiplex immunohistochemical (mIHC). <b>Results</b>: Comprehensive analysis indicates that the mutation rate of RA metabolism related genes in bladder cancer is about 20%, with significant gene amplification observed in <i>RDH10</i> and <i>CYP26B1.</i> We identified a group of subsets with significantly increased RA metabolism activity in bladder cancer tumor epithelial cells and found that this subgroup was significantly associated with poor prognosis (p < 0.05). <i>CYP26B1</i> was identified as a potential therapeutic target. It was found that <i>CYP26B1</i> is significantly correlated with tumor stemness and differentiation. <i>In vitro</i> experiments confirmed that overexpression of <i>CYP26B1</i> can significantly enhance the proliferation and migration of tumor cells. <b>Conclusion:</b> These results suggest that CYP26B1 may be closely related to the remodeling of the tumor microenvironment and may become a potential therapeutic target for bladder cancer.</p>","PeriodicalId":15183,"journal":{"name":"Journal of Cancer","volume":"16 8","pages":"2476-2491"},"PeriodicalIF":3.3,"publicationDate":"2025-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12170498/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144325873","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}
Journal of CancerPub Date : 2025-04-21eCollection Date: 2025-01-01DOI: 10.7150/jca.111585
Donggang Xu, Yue Zhang, Maoqia Shen, Xiaolong Cao
{"title":"A Comprehensive Analysis of the Role of DSN1 in Pan-Cancer Prognosis and Immunotherapy.","authors":"Donggang Xu, Yue Zhang, Maoqia Shen, Xiaolong Cao","doi":"10.7150/jca.111585","DOIUrl":"10.7150/jca.111585","url":null,"abstract":"<p><p><b>Background:</b> Dosage Suppressor of NNF1 (DSN1) is a component of the MIS12 kinetochore complex crucial in the cell cycle process. Recent evidence indicates its close association with cancer progression. The study aims to further explore DSN1's role in cancer. <b>Methods:</b> Using public databases, we investigated the expression patterns of DSN1 in mRNA, protein, and single-cell sequencing data across cancer types. Prognostic associations were assessed through survival analysis, and gene mutation frequencies were compared between high and low DSN1 expression groups. Gene set enrichment analysis was conducted to identify relevant biological pathways. We also examined the correlation of DSN1 with DNA methylation, tumor mutation burden (TMB), microsatellite instability (MSI), immune infiltration, and immune-regulatory genes. <b>Results:</b> Our analysis revealed that DSN1 is consistently overexpressed in tumor cells and actively dividing cells compared to normal tissues. The overexpression of DSN1 showed a significant correlation with either poor or favorable prognosis, depending on the cancer type. Notably, cancers such as COAD, LUAD, and UCEC exhibited high mutation and amplification frequencies in the DSN1-high group. Gene set enrichment analysis identified cell cycle-related pathways as the most significantly associated with DSN1 expression. Furthermore, DSN1 expression was positively correlated with DNA methylation, TMB, and MSI in most cancers. DSN1 was also closely associated with tumor-infiltrating immune cells and immune-regulatory genes, as well as immune therapy response and drug sensitivity. <b>Conclusion:</b> Our findings highlight the importance of DSN1 in tumorigenesis, progression, and immune therapy across various cancer types. Further studies are needed to explore its specific applications in individual cancer types.</p>","PeriodicalId":15183,"journal":{"name":"Journal of Cancer","volume":"16 8","pages":"2449-2465"},"PeriodicalIF":3.3,"publicationDate":"2025-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12170500/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144325846","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}
Journal of CancerPub Date : 2025-04-21eCollection Date: 2025-01-01DOI: 10.7150/jca.98431
Wenqiu Zhao, Tao Jin, Yun Liu, Shihe Shao, Feilun Cui
{"title":"High MIG-6 expression promotes tumor proliferation and metastasis of gastric cancer.","authors":"Wenqiu Zhao, Tao Jin, Yun Liu, Shihe Shao, Feilun Cui","doi":"10.7150/jca.98431","DOIUrl":"10.7150/jca.98431","url":null,"abstract":"<p><p><b>Background:</b> Mitogen-inducible gene-6 (<i>MIG-6</i>) is a feedback inhibitor that targets activated epidermal growth factor receptor (EGFR) and suppresses tumor growth fueled by constitutively activated EGFR. Nevertheless, the action mechanism of <i>MIG-6</i> in gastric cancer (GC) remains to be elucidated. <b>Methods:</b> Western blotting, fluorescence quantitative PCR, and immunohistochemistry were performed to detect the expression of <i>MIG-6</i> in GC cell lines and tissues. Public databases were used to analyze <i>MIG-6</i> in patients with GC. Furthermore, the GC cell lines were selected for the knockdown and overexpression of <i>MIG-6</i>. <b>Results:</b> Bioinformatics and histological analyses showed that <i>MIG-6</i> was elevated in human GC tissues and cells. The Kaplan-Meier plotter showed that patients with elevated MIG-6 expression had significantly shorter survival. Furthermore, small interference RNA-mediated reduction of <i>MIG-6</i> expression decreased EGFR/AKT signaling, as well as the proliferation and metastasis of human GC cells <i>in vitro</i>, whereas its overexpression increased these actions. Also, <i>MIG-6</i> overexpression promoted the epithelial-mesenchymal transition of GC cells as well as the expression of the migration-associated protein matrix metalloproteinase-9 <i>in vitro</i>. <b>Conclusion:</b> These results suggest that <i>MIG-6</i> can serve as a new prognostic biomarker or potential therapeutic target for the identification of patients with poor survival.</p>","PeriodicalId":15183,"journal":{"name":"Journal of Cancer","volume":"16 8","pages":"2466-2475"},"PeriodicalIF":3.3,"publicationDate":"2025-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12170504/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144325851","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}
Journal of CancerPub Date : 2025-04-21eCollection Date: 2025-01-01DOI: 10.7150/jca.102131
Paula Sawerska, Aneta Konwerska, Łukasz Galus, Agata Kolecka-Bednarczyk, Karolina Buszka, Damian Rusek, Agnieszka Seraszek-Jaros, Michał Nowicki, Jacek Mackiewicz, Joanna Budna-Tukan
{"title":"Pair-matched analysis of Circulating Melanoma Cells (CMCs) before and after Immunotherapy in Relation to other Melanoma-Specific Biomarkers.","authors":"Paula Sawerska, Aneta Konwerska, Łukasz Galus, Agata Kolecka-Bednarczyk, Karolina Buszka, Damian Rusek, Agnieszka Seraszek-Jaros, Michał Nowicki, Jacek Mackiewicz, Joanna Budna-Tukan","doi":"10.7150/jca.102131","DOIUrl":"10.7150/jca.102131","url":null,"abstract":"<p><p>Melanoma remains challenging in terms of diagnosis and treatment, and there is an urgent need to implement accurate diagnostic methods and personalized treatment to improve clinical outcomes. Therefore, it may be useful to enrich the panel of melanoma markers already in use and develop combinations of biomarkers for disease prognosis and monitoring. Data suggest that a promising biomarker for such a combination is circulating melanoma cells (CMCs). Although the relevances of various biomarkers in diagnosis, prognosis and treatment monitoring in melanoma have been extensively studied, we aimed at comprehensive investigation and comparison of liquid biopsy and tissue biomarkers with clinical status of the patient. Specifically, we focused on CMCs, by comparing the number of CMCs, including pre- and post-treatment. Furthermore, we have assessed the expression of the PMEL and Melan-A markers and the S100B and TIMP-1 protein levels in representative blood samples from melanoma patients and healthy controls. The number of CMCs in the study group was significantly higher than in the CMC-negative control group. However, there was no significant difference between the incidence of CMCs in the pre- and post-treatment blood draws. Nonetheless, we have observed a negative correlation between LDH levels and PFS, and a negative correlation between S100B levels and lymphocyte counts. The results of the study indicate that combinations of biomarkers, rather than any single biomarker alone, possess the highest clinical application potential, which urges further research on larger patient groups.</p>","PeriodicalId":15183,"journal":{"name":"Journal of Cancer","volume":"16 8","pages":"2421-2433"},"PeriodicalIF":3.3,"publicationDate":"2025-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12170499/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144325867","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":"circSLC39A8 by sponging hsa-miR-11181-5p and direct binding to PIK3CA mRNA promotes retinoblastoma proliferation.","authors":"Jian Gong, Zicheng Song, Jiandong Pan, Xiangwei Huang, Xiaofen Feng, Qian Li","doi":"10.7150/jca.99599","DOIUrl":"10.7150/jca.99599","url":null,"abstract":"<p><p><b>Background:</b> Retinoblastoma (RB) is a prevalent intraocular malignant tumor, posing a significant threat to human life and health. Although the involvement of circRNAs in various malignancies has been reported, their precise role in RB remains incompletely understood. <b>Methods:</b> High-throughput sequencing was utilized to construct differential expression profiles of circRNAs, followed by candidate gene screening using RT-qPCR. The circular structure of circSLC39A8 was confirmed through stability assays with RNase R and Act D. A research system for transiently silencing and overexpressing circSLC39A8 was established, with flow cytometry employed to assess cell cycle and apoptosis levels. Bioinformatics analyses, RT-qPCR, and western blot experiments were conducted to evaluate the expression of circSLC39A8, hsa-miR-11181-5p, and PIK3CA. RNA antisense purification experiments were performed to elucidate interactions among circSLC39A8, hsa-miR-11181-5p, and PIK3CA. <b>Results:</b> Our findings revealed a significant upregulation of circSLC39A8 in RB. Functionally, circSLC39A8 was identified as promoting cellular proliferation and suppressing apoptosis <i>in vitro</i>, thereby facilitating RB progression. Mechanistically, circSLC39A8 indirectly augmented the expression levels of PIK3CA mRNA by acting as a competitive endogenous RNA for hsa-miR-11181-5p, consequently enhancing the stability of PIK3CA mRNA and ultimately fostering RB cell proliferation while inhibiting apoptosis.</p>","PeriodicalId":15183,"journal":{"name":"Journal of Cancer","volume":"16 8","pages":"2434-2448"},"PeriodicalIF":3.3,"publicationDate":"2025-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12170501/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144325847","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}
Journal of CancerPub Date : 2025-04-13eCollection Date: 2025-01-01DOI: 10.7150/jca.106902
Sachin Kumar, Chung-Che Wu, Fitria Sari Wulandari, Chung-Chieh Chiao, Ching-Chung Ko, Hung-Yun Lin, Juan Lorell Ngadio, Cathleen Rebecca, Do Thi Minh Xuan, Dahlak Daniel Solomon, Michael Michael, Lidya Kristiani, Jian-Ying Chuang, Ming-Cheng Tsai, Chih-Yang Wang
{"title":"Integration of multi-omics and single-cell transcriptome reveals mitochondrial outer membrane protein-2 (MTX-2) as a prognostic biomarker and characterizes ubiquinone metabolism in lung adenocarcinoma.","authors":"Sachin Kumar, Chung-Che Wu, Fitria Sari Wulandari, Chung-Chieh Chiao, Ching-Chung Ko, Hung-Yun Lin, Juan Lorell Ngadio, Cathleen Rebecca, Do Thi Minh Xuan, Dahlak Daniel Solomon, Michael Michael, Lidya Kristiani, Jian-Ying Chuang, Ming-Cheng Tsai, Chih-Yang Wang","doi":"10.7150/jca.106902","DOIUrl":"https://doi.org/10.7150/jca.106902","url":null,"abstract":"<p><p>Lung adenocarcinoma (LUAD) remains to be one of the most prevalent and highly invasive forms of cancer. Mitochondrial outer membrane protein-2 or Metaxin-2 (MTX2), a key regulator of mitochondrial function, has been linked to cellular bioenergetics and stress response mechanisms. However, its roles in the progression and prognosis of LUAD remain largely unexplored. This study, employed a multi-omics approach, integrating transcriptomic and clinical patient data from public databases, to evaluate the expression and prognostic relevance of MTX2 in LUAD. Single-cell RNA sequencing was utilized to further explore MTX2's role in immune infiltration and interactions within the tumor microenvironment. Additionally, we validated these findings through a series of molecular biology and functional assays. Our results demonstrated that MTX2 expression was higher in LUAD tissues compared to normal lung tissues. Elevated MTX2 levels were significantly associated with poorer overall survival in LUAD patients. Functional analyses revealed that MTX2 regulates mitochondrial bioenergetics and facilitates tumor cell proliferation. Additionally, MTX2 expression was associated with increased immune cell infiltration. A pathway analysis identified cell metabolic and tumor growth pathways regulated by MTX2, supporting its role in tumor progression. Our research identifies MTX2 as a promising prognostic biomarker and therapeutic target for LUAD. Increased expression of MTX2 promotes tumor growth by altering metabolic pathways and modulating the immune response, underscoring its potential as a new target for LUAD treatment.</p>","PeriodicalId":15183,"journal":{"name":"Journal of Cancer","volume":"16 7","pages":"2401-2420"},"PeriodicalIF":3.3,"publicationDate":"2025-04-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12036103/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143982288","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":"Construction of a Prognostic Model based on CSC-related Genes in Patients with Colorectal Cancer.","authors":"Zi-Yue Li, Ming-Feng Li, Ying-Ying He, Guan-Sheng Zheng, Jie-Rong Chen, Yun-Miao Guo, Qizhou Lian, Cai-Feng Yue","doi":"10.7150/jca.108188","DOIUrl":"https://doi.org/10.7150/jca.108188","url":null,"abstract":"<p><p>Colorectal cancer (CRC) is one of the most common and deadly malignancies. Lack of efficient biomarkers for prognosis has limited the improvement of survival outcome in patients with CRC. Numerous studies have demonstrated the important roles of cancer stem cells (CSCs) in both treatment resistance and disease recurrence of CRC. Thus, the current study aims to construct a prognostic model based on expression level of CSC-related genes for precise molecular subtyping of CRC patients with different prognoses, TME infiltration patterns and therapeutic responses. The RNA sequencing data and clinical information were obtained from UCSC Xena database, followed by identification of differential expressed genes, univariate Cox regression, and LASSO regression to identify prognostic CSC-related genes and construct a novel prognostic risk scoring model consisting of 21 CSC-related genes. The patients in high-risk group suffered poor survival outcome (<i>P</i><0.0001). Moreover, the performance of CSC-related prognostic model was validated in individual GEO datasets including GSE41258 and GSE39582 (<i>P</i><0.05). Furthermore, patients with high-risk score exhibited lower response rate to immune checkpoint inhibitors as compared to those in low-risk group (17.4% vs. 28.2%), indicating the potential of CSC-related prognostic model to predict the immunotherapy response. Collectively, our findings provide an effective model to predict the immunotherapy response and survival outcome in patients with CRC.</p>","PeriodicalId":15183,"journal":{"name":"Journal of Cancer","volume":"16 7","pages":"2375-2387"},"PeriodicalIF":3.3,"publicationDate":"2025-04-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12036084/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143967915","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}
Journal of CancerPub Date : 2025-04-13eCollection Date: 2025-01-01DOI: 10.7150/jca.103286
Qiang Xue, Ruicong Ma, YueYuan Chen, Xiaodi Yan, Jiajia Liu, Jianhua Xue, Yang Yang, Xianchen Liu
{"title":"MiR-371b-5p reduces osteosarcoma cell migration and proliferation to induce apoptosis by targeting FUT4.","authors":"Qiang Xue, Ruicong Ma, YueYuan Chen, Xiaodi Yan, Jiajia Liu, Jianhua Xue, Yang Yang, Xianchen Liu","doi":"10.7150/jca.103286","DOIUrl":"https://doi.org/10.7150/jca.103286","url":null,"abstract":"<p><p>In our previous study (PMID: 34671604), we found that miR-317b-5b not only exerted anti-tumor effect, but also downregulated FUT4 expression in human myeloma cell line 143B. This study aims to investigate the biological function of miR-371b-5p in osteosarcoma progression and the role of FUT4 in this process. For <i>in vitro</i> investigations, the human osteosarcoma cell lines (SaOS2, 143B, KHOS and U2OS) as well as the human osteoblast cell line (hFOB1.19) were employed as models. The QRT-PCR assay was utilized to determine the relative amounts of miR-371b-5p and FUT4 expression in the cells. The functions and effects of miR-371b-5p on the abilities to proliferate, migrate, apoptosis and invade of KHOS and U2OS in osteosarcoma cells were investigated using assays including CCK-8, colony formation, EDU, wound-healing, Western blot, TUNEL and Transwell assay. The correlations between miR-371b-5p, its downstream gene FUT4 and its potential mechanisms in mediating osteosarcoma progression were explored with the assistance of dual-luciferase reporter analysis together with rescue experiments. MiR-371b-5p was less expressed in osteosarcoma cells compared with osteoblasts. Its overexpression significantly inhibited the abilities to proliferate, invade and migrate to promote apoptosis of osteosarcoma cells. The correlations between FUT4 and miR-371b-5p was established by the gene analysis of the dual-luciferase reporter analysis. FUT4 expression was dramatically decreased after the process of miR-371b-5p mimics being transfected into KHOS and U2OS cells. Additionally, overexpression of FUT4 induced osteosarcoma cell apoptosis and partially overcame miR-371b-5p's inhibitory effects on osteosarcoma cell's abilities to proliferate, invade and migrate. Osteosarcoma cells exhibit down-regulation of miR-371b-5p, that prevents osteosarcoma cells from proliferating, invading and migrating in order to promote osteosarcoma cell apoptosis through concentrating on the breakdown of FUT4.</p>","PeriodicalId":15183,"journal":{"name":"Journal of Cancer","volume":"16 7","pages":"2388-2400"},"PeriodicalIF":3.3,"publicationDate":"2025-04-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12036107/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143985178","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":"Identification of the role of MED6 in the development and prognosis of lung adenocarcinoma based on multi-omics profiling.","authors":"Changqing Yang, Ding Cheng, Shuo Wang, Baichuan Wang, Yingxi Li, Guixin Wang, Xingkai Wang, Cangchang Shi, Yao Tian, Keyun Zhu, Jing Feng","doi":"10.7150/jca.110981","DOIUrl":"https://doi.org/10.7150/jca.110981","url":null,"abstract":"<p><p><b>Background:</b> Lung adenocarcinoma (LUAD) is the most common subtype of lung cancer. Recent studies have highlighted the importance of Mediator complex subunits in cancer, but their specific roles in LUAD are still unclear. <b>Methods:</b> The CRISPR-Cas9 loss-of-function data was used to assess gene dependency in cell growth. RNA-seq data were analyzed to evaluate the prognostic value of Mediator subunits and explore their downstream pathways. Single-cell sequencing data were utilized to examine the tumor microenvironment in LUAD. A drug sensitivity analysis was performed to identify potential therapeutic options. <b>Results:</b> Mediator complex subunit 6 (MED6) was found to influence tumor cell growth in LUAD. Additionally, MED6 expression levels were associated with patient prognosis. MED6-positive tumor cells showed more active interactions with other cells in the LUAD microenvironment, promoting tumor progression. Based on MED6 expression, drugs such as paclitaxel, afatinib, and brivanib were identified as potential treatments. <b>Conclusions:</b> This study revealed the role of MED6 in LUAD and its potential as a biomarker. Our findings suggest that MED6 has an effect on LUAD progression and provide valuable insights for patient stratification and personalized treatment strategies.</p>","PeriodicalId":15183,"journal":{"name":"Journal of Cancer","volume":"16 7","pages":"2362-2374"},"PeriodicalIF":3.3,"publicationDate":"2025-04-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12036094/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144009208","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":"Erratum: Co-delivery of Cyclopamine and Doxorubicin Mediated by Bovine Serum Albumin Nanoparticles Reverses Doxorubicin Resistance in Breast Cancer by Down-regulating P-glycoprotein Expression: Erratum.","authors":"Yong-Lin Lu, Ya-Bin Ma, Chan Feng, Dong-Lei Zhu, Jie Liu, Lv Chen, Shu-Jing Liang, Chun-Yan Dong","doi":"10.7150/jca.113959","DOIUrl":"https://doi.org/10.7150/jca.113959","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.7150/jca.30323.].</p>","PeriodicalId":15183,"journal":{"name":"Journal of Cancer","volume":"16 7","pages":"2360-2361"},"PeriodicalIF":3.3,"publicationDate":"2025-04-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12036104/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143992218","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}