Cancer Cell International最新文献

{"title":"Correction: Human peritoneal fluid exerts ovulation- and nonovulation-sourced oncogenic activities on transforming fallopian tube epithelial cells.","authors":"Che-Fang Hsu, Vaishnavi Seenan, Liang-Yuan Wang, Pao-Chu Chen, Dah-Ching Ding, Tang-Yuan Chu","doi":"10.1186/s12935-025-03718-w","DOIUrl":"10.1186/s12935-025-03718-w","url":null,"abstract":"","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"98"},"PeriodicalIF":5.3,"publicationDate":"2025-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11909898/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143633805","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Molecular mechanisms of miR-192 in cancer: a biomarker and therapeutic target.","authors":"Yang Yang, Siti Razila Abdul Razak, Ida Shazrina Ismail, Yanxia Ma, Muhammad Amir Yunus","doi":"10.1186/s12935-025-03666-5","DOIUrl":"10.1186/s12935-025-03666-5","url":null,"abstract":"<p><p>Cancer remains a major global health challenge due to its rising prevalence and high mortality rates. The field of microRNAs (miRNAs) has made significant progress in the understanding of tumorigenesis and has broadened our knowledge of their targeting, especially in cancer therapy. miRNAs, a class of small non-coding RNAs, participate in post-transcriptional gene regulation by translational inhibition or mRNA degradation. Among these, microRNA-192 (miR-192) is located on human chromosome 11q13.1, and is highly correlated with the occurrence and development of various human cancers. Dysregulation of miR-192 has been extensively studied in various pathological processes, including tumorigenesis, making it a valuable biomarker for cancer diagnosis and prognosis. The functional role of miR-192 varies across cancer types, acting as either a tumor suppressor or as an oncogene through the modulation of multiple gene expressions and downstream signaling pathways. However, the roles of miR-192 in cancer appear inconsistent across types, with current research often focused on specific genes or pathways, limiting insight into its broader impact on cellular signaling networks. Therefore, this review aims to provide a comprehensive overview of miR-192 research. The paper reviews differences in miR-192 expression in cancer and systematically summarizes the role of miR-192 in cancers. The review further explores the complex roles of miR-192 in various pathological processes, emphasizing its regulatory pathways, interaction networks, and association with tumor progression. This review also illustrates the clinical application of miR-192 as a diagnostic and prognostic biomarker for non-invasive cancer detection, as it is consistently present in both serum and exosomes. A comprehensive summary and analysis of the relationship between miR-192 and various cancers may provide valuable insights, potentially guiding novel approaches in clinical diagnosis, therapeutic strategies, and foundational cancer research.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"94"},"PeriodicalIF":5.3,"publicationDate":"2025-03-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11908092/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143633821","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Single-cell transcriptomic analyses reveal heterogeneity and key subsets associated with survival and response to PD-1 blockade in cervical squamous cell carcinoma.","authors":"Xia Li, Zhao Zhao, Yanmei Cheng, Jiaqin Yan, Fang Ren, Yanyan Jia, Juanhua Li, Binhui Wang, Junqi Liu, Chenyin Wang, Meimei Gao, Hao Gu, Mingliang Fan, Huirong Shi, Mei Ji, Qitai Zhao","doi":"10.1186/s12935-025-03725-x","DOIUrl":"10.1186/s12935-025-03725-x","url":null,"abstract":"<p><strong>Background: </strong>Understanding the intricate tumor microenvironment (TME) is crucial for elucidating the mechanisms underlying the progression of cervical squamous cell carcinoma (CSCC) and its response to anti-PD-1 therapy.</p><p><strong>Methods: </strong>In this study, we characterized 50,649 cells obtained from the CSCC for single-cell RNA sequencing and integrated bulk sequencing data from The Cancer Genome Atlas (TCGA) and clinical samples to explore their cell composition, metabolic processes, signaling pathways, specific transcription factors, lineage tracking and response to immunotherapy. In vivo experiments were performed to validate the function of key cell subsets.</p><p><strong>Results: </strong>We identified ten major cell type and 35 subsets of stromal and immune cells in TME and observed distinct patterns in the metabolic processes and signaling pathways of these cells between tumor and normal tissues. Furthermore, PCNA clamp-associated factor (PCLAF)⁺ tumor-associated epithelial cell (TAEpis) was negatively correlated with the number of C-X-C motif chemokine ligand 13 (CXCL13)⁺ CD8⁺ T cells, overall survival, and response to anti-programmed cell death-1(PD-1) therapy in patients with CSCC. Both in vivo and in vitro experiments demonstrated that PCLAF⁺ TAEpis promotes the apoptosis of CD8⁺ T and tumor growth, while also inhibiting T cell infiltration and function.</p><p><strong>Conclusion: </strong>Our findings illuminate the heterogeneity of the complex TME in CSCC and offer evidence supporting PCLAF⁺ TAEpis as a promising therapeutic target.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"90"},"PeriodicalIF":5.3,"publicationDate":"2025-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11907857/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143623618","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploring the potential mechanisms of sorafenib resistance in hepatocellular carcinoma cell lines based on RNA sequencing.","authors":"Minghui Sun, Zhi Zhang, Chunyan Chen, Juan Zhong, Zhongrong Long, Ling Shen, Hai Huang, Jianxun Lu","doi":"10.1186/s12935-025-03728-8","DOIUrl":"10.1186/s12935-025-03728-8","url":null,"abstract":"<p><strong>Background: </strong>Exploring the mechanisms underlying sorafenib resistance that arises in hepatocellular carcinoma (HCC) may provide new treatment perspectives.</p><p><strong>Methods: </strong>Drug-resistant and drug-sensitive HCC cell lines were constructed from existing HepG2 and Huh7 cell lines, and gene expression profiles were determined. Genes differentially expressed between the resistant and sensitive lines were identified and organized into modules based on weighted gene co-expression network analysis. Pathways and biological processes involving the module genes were explored and validated using gene set enrichment analysis. By analyzing the expression differences of Long non-coding ribonucleic acid (RNAs), microRNAs (miR), circular RNAs, and messenger RNAs between drug-resistant and sensitive cell lines, a gene regulatory network was constructed to reveal the mechanism of sorafenib resistance. In addition, we also analyzed the correlation between the candidate sorafenib resistance gene and the survival of patients with liver cancer.</p><p><strong>Results: </strong>Our analyses suggested that sorafenib resistance could arise when the circular RNA circ_SPECC1 regulated the microRNA hsa-let-7c-5p, which in turn regulated the cell cycle proteins cyclin-dependent kinase 1 and polo-like kinase 1, as well as interleukin 13 receptor, alpha 1 in the Janus kinase-signal transducer (JAK-STAT) and activator of transcription signaling pathway. Patient survival was associated with miR-18a-z and mitogen-activated protein kinase kinase 4 levels.</p><p><strong>Conclusions: </strong>Sorafenib resistance in HCC may involve the circ_SPECC1, hsa-let-7c-5p, cell cycle, and JAK-STAT signaling pathways. These insights may guide future efforts to mitigate or prevent such resistance.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"91"},"PeriodicalIF":5.3,"publicationDate":"2025-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11907981/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143623615","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SERPINI1 serves as a biomarker promoting cell proliferation and invasion in hepatocellular carcinoma.","authors":"Yawei Han, Gaoyv Wang, Erwei Han, Shuting Yang, Ran Zhao, Yvying Lan, Meng Zhao, Yueguo Li, Li Ren","doi":"10.1186/s12935-025-03716-y","DOIUrl":"10.1186/s12935-025-03716-y","url":null,"abstract":"<p><strong>Background: </strong>SERPINI1 is a protein-coding gene, which has been reported to be related to malignancies, and the encoding protein is a secreted protein. Nevertheless, the specific effect of SERPINI1 on Hepatocellular carcinoma (HCC) remains unclear.</p><p><strong>Methods: </strong>The expression level of SERPINI1 in cancers was detected by the Gene Expression Omnibus (GEO) database, the Gene Expression Profiling Interactive Analysis (GEPIA) database and the collected serum of HCC patients. The receiver operating characteristic (ROC) curve and area under curve (AUC) were used to evaluate the diagnostic effectiveness of serum SERPINI1 and the combination of AFP and SERPINI1 for HCC. The Kaplan-Meier (KM) survival was used to evaluate the prognostic capacity of SERPINI1 for HCC in GEPIA database. Furthermore, the correlations between clinicopathological characteristics and the level of serum SERPINI1 were analyzed. Besides, we detected the expression of SERPINI1 in HepG2 by qPCR and western blot, and confirmed the biological function of SERPINI1 through MTT, EdU, wound healing and transwell invasion assay.</p><p><strong>Results: </strong>The results indicated that the level of SERPINI1 was significantly increased in tissue and serum of HCC patients. ROC analysis displayed that SERPINI1 had a significantly diagnostic value for HCC, the combination of AFP and SERPINI1 gained the higher specificity and sensitivity. The KM survival curves indicated that patients with SERPINI1 overexpression had worse overall survival. Furthermore, we found the positive correlations between serum SERPINI1 level and some clinicopathological characteristics, such as tumor size, differentiation degrees and so on. In addition, in vitro experiments revealed that SERPINI1 could promote the proliferation and invasion of HCC.</p><p><strong>Conclusions: </strong>Taken together, our study demonstrates that SERPINI1, which is highly expressed in HCC and closely related to cell proliferation and invasion, may serve as a novel biomarker for diagnosis and prognosis of HCC.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"88"},"PeriodicalIF":5.3,"publicationDate":"2025-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11908049/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143623617","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction: LncRNA CRNDE promotes hepatoma cell proliferation by regulating the metabolic reprogramming of M2 macrophages via ERK pathway.","authors":"Chao Lin, Tao Jiang, Changyong E, Lun Wang, Tong Chen, Xia Wang, Yien Xiang","doi":"10.1186/s12935-025-03719-9","DOIUrl":"10.1186/s12935-025-03719-9","url":null,"abstract":"","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"93"},"PeriodicalIF":5.3,"publicationDate":"2025-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11907828/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143623673","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Amino acid metabolism in glioblastoma pathogenesis, immune evasion, and treatment resistance.","authors":"Shriyansh Srivastava, Robab Anbiaee, Mohammad Houshyari, Laxmi, Sathvik Belagodu Sridhar, Sumel Ashique, Sadique Hussain, Sachin Kumar, Tahreen Taj, Zeinab Akbarnejad, Farzad Taghizadeh-Hesary","doi":"10.1186/s12935-025-03721-1","DOIUrl":"10.1186/s12935-025-03721-1","url":null,"abstract":"<p><p>Glioblastoma (GBM) ranks among the most lethal primary tumors of the central nervous system. This is partly due to its complex intracellular metabolism and interactions with the surrounding tumor microenvironment (TME). Compelling evidence represents that altered amino acids (AAs) metabolism plays a crucial role in both areas. The role of AAs and their metabolites in glioma biology is an emerging topic. Therefore, this review was conducted to summarize the current knowledge about the molecular mechanisms by which AAs participate in the GBM pathogenesis. AAs can directly influence tumor progression by affecting tumor cell metabolism or indirectly by releasing bioactive agents through particular metabolic pathways. This review begins by examining the metabolic pathways of essential AAs, such as tryptophan, tyrosine, and phenylalanine, which contribute to synthesizing critical neurotransmitters and shape tumor metabolism signatures. We explore how these pathways impact tumor growth and immune modulation, focusing on how AAs and their metabolites can promote malignant properties in GBM cells. AAs also play a pivotal role in reprogramming the TME, contributing to immune evasion and resistance to therapy. The review further discusses how tumor metabolism signatures, influenced by AA metabolism, can enhance the immunosuppressive microenvironment, providing new avenues for targeted immunotherapies. Finally, we outline potential therapeutic strategies to modulate AA metabolism and emphasize critical opportunities for future research to improve GBM management.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"89"},"PeriodicalIF":5.3,"publicationDate":"2025-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11908050/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143623672","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction Note: Circular RNA ATXN7 promotes the development of gastric cancer through sponging miR-4319 and regulating ENTPD4.","authors":"Zhen Zhang, Honglei Wu, Zhaosheng Chen, Guangchun Li, Bin Liu","doi":"10.1186/s12935-025-03733-x","DOIUrl":"10.1186/s12935-025-03733-x","url":null,"abstract":"","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"92"},"PeriodicalIF":5.3,"publicationDate":"2025-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11908004/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143623616","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"DUSP4 inhibited tumor cell proliferation by downregulating glycolysis via p-ERK/p-PGK1 signaling in ovarian cancer.","authors":"Ying Xiong, Xiaoqian Zhang, Weiwei Xie, Yujia Yin, Yujing Qian, Xiang Ying, Xiaocui Zheng, Xipeng Wang","doi":"10.1186/s12935-025-03722-0","DOIUrl":"10.1186/s12935-025-03722-0","url":null,"abstract":"<p><p>Ovarian cancer (OC) remains a leading cause of gynecological cancer-related mortality, with poor prognosis and limited therapeutic options, underscoring the urgent need for a deeper understanding of OC biology. In this study, we identified a marked reduction in dual-specificity phosphatase 4 (DUSP4) expression in OC tissues compared to benign ovarian masses, with even further decreases observed in metastatic lesions. Moreover, DUSP4 expression varied among OC subtypes, with the lowest levels observed in serous ovarian cancer, and was associated with P53 and KI67 protein levels, altered TP53 mutation rates, advanced tumor stages, and poorer prognosis. Functional experiments demonstrated that DUSP4 overexpression suppressed OC cell proliferation, migration, and invasion in vitro. Phosphoproteomic profiling via LC-MS/MS analysis identified the MAPK pathway and cellular metabolism as key downstream targets of DUSP4. Notably, DUSP4 overexpression reduced phosphorylation of PGK1 at Ser203, a critical regulator of anaerobic glycolysis, and decreased its mitochondrial localization, leading to reduced lactate production and increased ROS levels. Mechanistically, DUSP4 dephosphorylated p-ERK, disrupting its interaction with PGK1 and subsequently reducing PGK1 S203 phosphorylation. In vivo, DUSP4 overexpression significantly inhibited tumor growth in mouse models, accompanied by decreased p-ERK and PGK1 S203 levels. These findings highlight a regulatory axis involving DUSP4, p-ERK, and PGK1, through which DUSP4 modulates glycolysis and tumor progression. This study establishes DUSP4 as a prognostic biomarker and a potential therapeutic target for OC, offering new insights into its role in tumor metabolism and growth.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"87"},"PeriodicalIF":5.3,"publicationDate":"2025-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11908039/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143623614","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Primary exploration of cell-free DNA in the plasma of patients with parathyroid neoplasms using next-generation sequencing.","authors":"Qingyuan Zheng, Ming Cui, Ou Wang, Xiaoyan Chang, Jinheng Xiao, Tianqi Chen, Mengyi Wang, Surong Hua, Ya Hu, Quan Liao","doi":"10.1186/s12935-025-03699-w","DOIUrl":"10.1186/s12935-025-03699-w","url":null,"abstract":"<p><strong>Background and aims: </strong>Plasma cell-free DNA (cfDNA) has been used to monitor gene mutations and diagnose tumors. Discriminating parathyroid carcinoma (PC) from parathyroid adenoma (PA) before surgery is difficult because of the overlap in clinical features between parathyroid neoplasms. We aimed to detect cfDNA mutations in plasma samples from PC and PA patients before surgery to predict the CDC73 status in tumor tissue and help in the differential diagnosis of parathyroid neoplasms.</p><p><strong>Materials and methods: </strong>Eighteen PC patients and 13 PA patients were enrolled. Plasma cfDNA was detected using next-generation sequencing, with DNA from matched peripheral white blood cells used as a control. CDC73 gene mutations were detected via whole-exome sequencing or parafibromin staining via immunohistochemistry of tumor tissues. Logistic regression was used to evaluate the ability of cfDNA mutations to predict the CDC73 status in tumor tissue and for differential diagnosis. CDC73 gene mutation or parafibromin staining loss were defined as CDC73 abnormalities.</p><p><strong>Results: </strong>One PC patient was not tested for CDC73 abnormalities due to the absence of tumor specimen. CDC73 abnormalities were not detected in all 13 PA patients, whereas 10 PC patients harboured CDC73 abnormalities in tumor specimens (P = 0.001). Among the 10 patients, CDC73 mutations were identified in the cfDNA of 8 patients. In another 20 patients without CDC73 abnormalities in tumors, CDC73 mutation was detected in the cfDNA of 4 patients. Using the CDC73 status in cfDNA, the area under the receiver operating characteristic curve (AUC) for predicting CDC73 abnormalities in tumor tissue was 0.80 (95% CI: 0.622-0.978), and the AUC for predicting malignancy was 0.795 (95% CI 0.632-0.958).</p><p><strong>Conclusion: </strong>This study is the first attempt to evaluate the gene mutation status of parathyroid neoplasms through the deep sequencing of plasma cfDNA, which could also help to identify PC prior to surgery.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"86"},"PeriodicalIF":5.3,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11905564/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143613498","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}