Cancer Cell International最新文献

{"title":"Mesenchymal stem cells and cancer stem cells promote colorectal cancer cell growth and biological functions via cell-cell indirect contact.","authors":"Yang Liu, Jianing Zhao, Bo Yang, Xu Yang, Juan Chen, Jinyang Cheng, Xiaoshuang Yuan, Guangyang Liu, Xiao Xu, Yanju Li, Dongxin Tang, Feiqing Wang","doi":"10.1186/s12935-025-03993-7","DOIUrl":"10.1186/s12935-025-03993-7","url":null,"abstract":"","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"344"},"PeriodicalIF":6.0,"publicationDate":"2025-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12506248/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145249770","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":"PD-L1 has a stronger effect on increasing headache risk than PD-1: a systematic review and meta-analysis.","authors":"Yuan Tian, Zixuan Feng, Feng Feng, Meng Fan, Yu Hu, Zhuoqi Li, Yuanyuan Wang, Kai Zhang, Qi Dang","doi":"10.1186/s12935-025-03911-x","DOIUrl":"10.1186/s12935-025-03911-x","url":null,"abstract":"<p><strong>Purpose: </strong>This meta-analysis aimed to clarify the risk of headaches caused by programmed cell death 1 (PD-1) and programmed cell death ligand 1 (PD-L1) inhibitors.</p><p><strong>Method: </strong>Relevant clinical trials were screened using PubMed. The risk of headache associated with PD-1 or PD-L1 inhibitors was calculated using the mirror principle and PRISMA guidelines.</p><p><strong>Results: </strong>A total of 33 clinical trials were screened for this comprehensive meta-analysis, yielding nine mirror-pairing groups. The risk of headache with PD-1 or PD-L1 inhibitors was significantly higher than that with placebo (OR = 1.48, 95% CI: [1.06, 2.06], Z = 2.33, P = 0.02) and similar to that with chemotherapy drugs (OR = 1.06, 95% CI: [0.84, 1.34], Z = 0.49, P = 0.62). When PD-1 or PD-L1 inhibitors are combined with other immune-related drugs, the risk of headaches increases to varying degrees. However, when combined with chemotherapy, this risk did not increase significantly (OR = 1.02, 95% CI: [0.78, 1.32], Z = 0.11, P = 0.91). Compared with PD-1, PD-L1 inhibitors were associated with a higher headache risk (OR = 1.39, 95% CI: [0.64, 2.12], Z = 1.51, P = 0.13).</p><p><strong>Conclusion: </strong>PD-L1 has a stronger effect on increasing headache risk than PD-1. Similar to the comparison of PD-1 or PD-L1 versus chemotherapy, PD-1 or PD-L1 plus chemotherapy did not significantly increase headache risk.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"341"},"PeriodicalIF":6.0,"publicationDate":"2025-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12506019/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145249865","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":"Interactions between LncRNAs and MAPK signaling pathways in the pathogenesis of breast cancer.","authors":"Baifang Ding, Xuguang Wang, Zhong Zhang, Yiwei Wang, Wei Bo, Mengyuan Zhang, Zitong Tian, Yaolu Wang, Xinyao Xue, Min Zhang","doi":"10.1186/s12935-025-03943-3","DOIUrl":"10.1186/s12935-025-03943-3","url":null,"abstract":"","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"339"},"PeriodicalIF":6.0,"publicationDate":"2025-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12502614/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145238012","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":"Regulatory role of N-nitroso compounds and lncRNA NEAT1 in endoplasmic reticulum stress and malignant transformation of gastric epithelial cells.","authors":"Xing Liu, Yichun Zhao, Yueyue Zhou, Xihuan Zou, Ruobing Chen, Yuting Peng, Meng Yu","doi":"10.1186/s12935-025-03954-0","DOIUrl":"10.1186/s12935-025-03954-0","url":null,"abstract":"<p><p>This study investigates the early oncogenic transformation of gastric epithelial cells (GES-1) and adenocarcinoma cells (AGS) following long-term exposure to N-nitroso compounds (NOCs), using N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) as a model carcinogen. Prolonged MNNG treatment enhanced proliferation, migration, invasion, and anchorage-independent growth. These effects were accompanied by persistent activation of endoplasmic reticulum stress (ERS) and autophagy, characterized by elevated PERK, eIF2α, ATF4, CHOP, Beclin-1, and LC3-II, and reduced p62. Long non-coding RNA nuclear-enriched abundant transcript 1 (NEAT1) was markedly upregulated and acted as a competing endogenous RNA, sponging microRNA-329-3p (miR-329-3p) to derepress ATF4. Silencing NEAT1 or restoring miR-329-3p expression suppressed ERS, autophagy, and malignant traits. These findings establish a NEAT1/miR-329-3p/ATF4 signaling axis that links stress response to early gastric epithelial transformation, offering a potential target for intervention.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"337"},"PeriodicalIF":6.0,"publicationDate":"2025-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12495730/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145225097","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":"A review of exercise-induced epigenetic modifications in prostate tissue: implications for gene expression and tumor progression in prostate cancer.","authors":"Keng Ye, Zunjin Ke, Weima Gesang, Ke Liang, Melika Malek","doi":"10.1186/s12935-025-03950-4","DOIUrl":"10.1186/s12935-025-03950-4","url":null,"abstract":"<p><p>Physical exercise is associated with a lower incidence and development of prostate cancer (PCa), according to epidemiologic research. In particular, it modifies the levels of endogenous hormones such as insulin, testosterone, and insulin-like growth factor. Moreover, physical exercise of various sorts and durations may affect the tumor microenvironment differently. There is growing evidence that physical exercise is associated with epigenetic alterations in prostate tissue, although its consequences on the prostate are yet unknown. It is well recognized that epigenetic changes, including DNA methylation and histone modifications, interfere with important biological functions in malignancies, including tumor development, tissue invasion, and metastasis, and they also increase the likelihood of genetic abnormalities. Notably, exercise has been shown to have anticancer, DNA methylation, histone, microRNA, lncRNA, and apoptosis-inducing properties. Exercise capacity to alter biomarkers of DNA methylation, histone changes, miRNA, lncRNA, and apoptotic induction makes predictive diagnostics possible, enabling patient stratification and early identification of at-risk patients. Thus, this review summarizes research on the molecular processes and therapeutic applications of exercise in prostate tissue, particularly in the context of prostate cancer.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"327"},"PeriodicalIF":6.0,"publicationDate":"2025-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12495689/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145225106","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":"Salivary genetic biomarkers of lung cancer: a systematic review and meta-analysis of the diagnostic accuracy.","authors":"Maryam Koopaie, Mahnaz Fatahzadeh, Sajad Kolahdooz","doi":"10.1186/s12935-025-03968-8","DOIUrl":"10.1186/s12935-025-03968-8","url":null,"abstract":"","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"332"},"PeriodicalIF":6.0,"publicationDate":"2025-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12495827/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145225108","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":"GRP-based vaccines as a novel approach in cancer immunotherapy: mechanisms, challenges, and prospects.","authors":"Razieh Malekian Shahreza, Hamed Zare, Nima Rastegar-Pouyani, Hamid Aria, Fatemeh Hakim, Mohammad Arefnia, Hamid Bakherad","doi":"10.1186/s12935-025-03979-5","DOIUrl":"10.1186/s12935-025-03979-5","url":null,"abstract":"<p><p>Glucose-regulated proteins (GRPs), key members of the heat shock protein (HSP) family, function as molecular chaperones that are upregulated under endoplasmic reticulum (ER) stress. Prominent GRPs such as GRP78, GRP94/gp96, GRP75, and GRP170 play a great role in cancer cell survival and progression by promoting protein folding, immune evasion, and resistance to therapy. Within the tumor microenvironment, which is characterized by hypoxia, acidosis, and nutrient deprivation, GRPs can facilitate critical processes including proliferation, angiogenesis, metastasis, and apoptotic resistance. Moreover, beyond their intracellular roles, GRPs have been found to possess considerable immunogenic potential when expressed on the cell surface or secreted. As a result, these findings have led to the development of GRP-based cancer vaccines that can elicit robust adaptive immune responses by chaperoning tumor antigens to antigen-presenting cells. Current evidence suggests GRP75 (HSPA9/mortalin) is less immediately tractable than ER-resident GRPs (78/94/170) for vaccine design, primarily owing to its mitochondrial localization and poor antigen accessibility. However, nanoparticle-mediated delivery or CRISPR-engineered surface expression could reposition it as a future target, pending advances in intracellular antigen presentation pathways. Preclinical models have demonstrated that GRP-based immunotherapy can induce cytotoxic T lymphocyte responses and tumor regression. Additionally, repurposing GRP-targeted strategies from infectious, autoimmune, and neurodegenerative disease contexts may offer promising translational avenues in the field of cancer. Despite encouraging results, challenges such as tumor heterogeneity, immune suppression, and delivery optimization have still remained. Therefore, future research should aim to increase antigen specificity, optimize vaccine formulations, and explore combinatory regimens to overcome resistance mechanisms in cancer cells. Overall, GRP-targeted vaccines represent a very compelling candidate in cancer immunotherapy with great potentials for clinical translation in the future.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"338"},"PeriodicalIF":6.0,"publicationDate":"2025-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12495762/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145225109","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":"Kaempferol triggers cellular senescence via CDK1 ubiquitination in HCC cells.","authors":"Damin Liang, Min Tian, Guomei Hu, Yu Zhang, Lunyou Zhang, Juqi Chen, Xin Shen, Huayong Jian, Peng Tian, Tingchao Li, Xiaoju Cheng","doi":"10.1186/s12935-025-03961-1","DOIUrl":"10.1186/s12935-025-03961-1","url":null,"abstract":"<p><p>Hepatocellular carcinoma (HCC) is a common malignancy with poor prognosis. Cellular senescence, a state linked to cell cycle arrest, represents a potential therapeutic strategy for cancer. However, the clinical impact and regulatory mechanism of cellular senescence in HCC remains incompletely unknown. We identified HCC associated differentially expressed genes (DEGs) using bioinformatics analysis of public databases (TCGA, GEO, GEPIA, etc.). Enrichment, prognostic, risk scoring models analyses revealed cyclin-dependent kinase 1 (CDK1) as a core senescence-related gene. CDK1 expression was upregulated in HCC tissues and correlated with poor prognosis of HCC patients. In addition, CDK1 knockdown significantly increased senescence markers (the level or activity of P16, P21, and SA-β-gal), and induced cellular senescence in HepG2 cells. Molecular docking demonstrated high-affinity binding between CDK1 and kaempferol (KAE; affinity = -9.7 kcal/mol). KAE treatment similarly increased senescence markers and promoted cellular senescence in HepG2 cells. Mechanistically, KAE reduced CDK1 protein levels by promoting its ubiquitination and subsequent degradation. These findings indicated that KAE might induce cellular senescence through CDK1 ubiquitination, providing potential drugs and targets for HCC treatment.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"325"},"PeriodicalIF":6.0,"publicationDate":"2025-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12495675/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145225148","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":"RPL22L1-Myc positive feedback loop drives lung adenocarcinoma progression.","authors":"Yahua Wu, Yingjiao Zhu, Rongqi Jiang, Weiwei Gu, Lihu Lu, Na Yao, Bin Du, Jinhuo Lai","doi":"10.1186/s12935-025-03945-1","DOIUrl":"10.1186/s12935-025-03945-1","url":null,"abstract":"<p><strong>Background: </strong>Ribosomal protein L22 like 1 (RPL22L1) plays an important role in some tumours. However, its role in lung adenocarcinoma (LUAD) is less studied. This study aimed to analyse the molecular mechanism of RPL22L1 in LUAD and to identify new targets for LUAD treatment.</p><p><strong>Methods: </strong>Real-time quantitative reverse transcription polymerase chain reaction (RT-qPCR) and Western blot (WB) were employed to detect the mRNA and protein expression, respectively. The CCK8 assay, colony formation assay, and transwell migration and invasion assay were utilized to assess the effects of RPL22L1 on LUAD cell proliferation, migration, and invasion. A nude mouse subcutaneous graft tumor model was used to evaluate the effect of RPL22L1 on the proliferative capacity of LUAD cells in vivo. Dual fluorescent reporter gene assays, ubiquitination immunoprecipitation assays, and protein degradation assays were conducted to explore the potential mechanism of RPL22L1 in LUAD.</p><p><strong>Results: </strong>The study demonstrated that RPL22L1 could promote the proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) of LUAD cells. Mechanistically, the upregulation of RPL22L1 in LUAD activated the MAPK/ERK/Myc signaling pathway, which subsequently promoted the proliferation, migration, invasion, and EMT of LUAD cells. Furthermore, RPL22L1 was found to influence the ubiquitination of Myc protein, inhibit its degradation, and maintain its stability. Additionally, Myc protein could directly bind to the promoter region (-653 to -664) of RPL22L1 and enhance its transcriptional expression, forming a positive feedback loop to promote the developmental process of LUAD.</p><p><strong>Conclusions: </strong>Our study revealed a positive feedback loop between RPL22L1 and Myc that drove LUAD progression.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"333"},"PeriodicalIF":6.0,"publicationDate":"2025-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12495810/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145225159","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":"Cellular and molecular features of acute myeloid leukemia investigation based on single-cell RNA sequencing.","authors":"Zheng-Fa Li, Jun-Rong Lu, Yun Dai, Rui-Jiao Mao, Yang-Liu Lu, Rong Sun, Jiao Liu, Lu-Lu Dong, Li-Ling Xia, Yun-Chao Xu, Tian Xia, Xiao Qin, Ting Dong","doi":"10.1186/s12935-025-03962-0","DOIUrl":"10.1186/s12935-025-03962-0","url":null,"abstract":"<p><p>Acute myeloid leukemia (AML) is defined as a highly heterogeneous clonal malignant disease of immature myeloid hematopoietic stem cells. The objective of this study was to identify the principal cell clusters in AML and their associated hub genes through the analysis of single-cell sequencing data. We present a comprehensive and valuable landscape of 58,717 cells and 27,311 genes derived from bone marrow samples obtained from 5 patients with AML and 3 controls. Then, 9 cell subclusters were identified. The ratios of common myeloid progenitor (CMP), Myelocyte, and Pro-Myelocyte were found to be significantly different between AML and control, as these cells were utilized as differential cells in the present study. A total of 26 differentially expressed genes were identified following the merging and de-weighting of the data. 4 hub genes, ELANE, LTF, S100A12, and SLPI, were selected for further analysis. Homogeneity analysis was conducted on the Myelocyte and Pro-Myelocyte cells, which were subsequently re-clustered into 11 and 8 cell clusters, respectively. In conclusion, we leveraged high-throughput single-cell transcriptomics to parse the cell landscape in the bone marrow from AML patients, 2 key cell types, myelocyte, and pro-myelocyte and related hub genes, ELANE, LTF, S100A12, SLPI were found, and biological functions, regulatory relationships, and developmental status of these key cells, as well as the biological pathways, the molecular regulatory mechanisms, and the related drugs, involved in the hub genes were demonstrated. Our data and findings provide novel insight into AML pathological development and can be inspired in the treatment of AML.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"326"},"PeriodicalIF":6.0,"publicationDate":"2025-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12495717/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145225096","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}