Cancer Cell International最新文献

{"title":"N7-methylguanosine (m7G) modification in breast cancer: clinical significances and molecular mechanisms.","authors":"Tianyao Yang, Chunyan Chen, Fangfang Wang, Lan Yue","doi":"10.1186/s12935-025-03859-y","DOIUrl":"10.1186/s12935-025-03859-y","url":null,"abstract":"<p><p>The therapeutic strategies for advanced breast cancer (BC) continue to present significant challenges. Consequently, the implementation of precise diagnostic biomarkers and prognostic targets is essential for effective BC management. Recently, N7-methylguanosine (m7G) modification has garnered considerable attention in the context of various cancer types. In this study, we conducted a comprehensive literature review to explore the potential role of m7G in the tumorigenesis of BC. Analysis of thirteen relevant studies revealed that m7G methyltransferases were usually aberrantly expressed in BC, including TNBC and breast invasive carcinoma. m7G modifications in mRNA, tRNA, and rRNA can ultimately affect the expression of target genes (i.e., m7G regulators [e.g., METTL1/WDR4], m7G-associated genes [e.g. P27 and AGO2], m7G-related lncRNAs [e.g., LINC01871 and LINC00115], and m7G-related miRNAs [e.g. miR-7 and miR-139]) and regulate BC-related biological functions. These novel insights indicate that m7G modification and its regulators hold significant potential for future clinical applications in the diagnosis and treatment of BC. In the future, how to apply m7G modifications to identify the implementation of clinically personalized BC treatment needs to be further explored.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"303"},"PeriodicalIF":6.0,"publicationDate":"2025-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12341331/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144834112","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":"Heme oxygenase-1 leads to cisplatin resistance in nasopharyngeal carcinoma by reducing oxidative stress and ferroptosis.","authors":"Zhongqiang Cheng, Lixian Huang, Yanshu Zhang, Kaiyue Yue, Shunmo Jia, Zhijie Fang, Zhiqiang Lin","doi":"10.1186/s12935-025-03908-6","DOIUrl":"10.1186/s12935-025-03908-6","url":null,"abstract":"<p><strong>Background: </strong>Nasopharyngeal carcinoma (NPC) is a malignancy with high a mortality rate. This study investigates the impact of heme oxygenase-1 (HO-1) in cisplatin (CDDP) resistance in NPC.</p><p><strong>Methods: </strong>The time-dependent effect of CDDP on two NPC cell lines (HK1 and C666-1) were investigated. CDDP-resistant cells were established by exposing the parental cells to increasing concentrations of CDDP. Parental cells received treatment of the HO-1 inducer Hemin while resistant cells received treatment of the HO-1 inhibitor ZnPP to explore the influence of HO-1 activity on CDDP resistance in NPC cell lines. Erastin was used to verify the effect of ferroptosis on CDDP sensitivity in cells. Parallel settings were performed in mouse xenograft tumor models for in vivo validation.</p><p><strong>Results: </strong>CDDP time-dependently reduced growth and mobility of NPC cells within the initial 48 h, but the cytotoxicity was no longer significantly enhanced afterward. HO-1 was upregulated in cells after CDDP treatment, showing correlation with acquired CDDP resistance. Inducing HO-1 activity in parental cells protected cells from oxidative damage, apoptosis, and ferroptosis, while suppressing HO-1 activity using ZnPP restored the therapeutic efficacy of CDDP in drug resistant cells. Moreover, the Erastin treatment also restored the cytotoxicity of CDDP to the resistant cells. In mice bearing xenograft tumors, treatment with either ZnPP or Erastin weakened the growth and weight of tumors.</p><p><strong>Conclusion: </strong>This work suggests that HO-1 is pertinent to acquired CDDP resistance in NPC cells by suppressing oxidative stress and ferroptosis.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"302"},"PeriodicalIF":6.0,"publicationDate":"2025-08-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12337500/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144820622","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":"Predicting survival of persons with newly-diagnosed multiple myeloma.","authors":"Limei Zhang, Yun Wang, Robert Peter Gale, Yang Liang","doi":"10.1186/s12935-025-03916-6","DOIUrl":"10.1186/s12935-025-03916-6","url":null,"abstract":"","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"301"},"PeriodicalIF":6.0,"publicationDate":"2025-08-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12335180/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144811834","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":"Multi-omics profiling of metastatic colorectal cancer reveals the transcriptional network of focal adhesion and immune suppression and the role of p-RPS6.","authors":"Yimei Jiang, Zhe Li, Fang Zheng, Wenqing Jia, Zichao Guo, Zhuoqing Xu, Chenhao Huang, Zhiliang Li, Changgang Wang, Kun Liu, Haoran Feng, Ren Zhao, Xi Cheng","doi":"10.1186/s12935-025-03924-6","DOIUrl":"10.1186/s12935-025-03924-6","url":null,"abstract":"<p><strong>Background: </strong>Colorectal cancer (CRC) is one of the deadliest malignancies worldwide characterized by rapid progression, high metastasis propensity. Our study aimed to identify the driving biological factors of metastatic CRC.</p><p><strong>Methods: </strong>We obtained frozen tumor tissues of 8 metastatic CRC (mCRC) patients and 10 non-metastatic CRC (nmCRC) patients from Ruijin Hospital for proteome analysis. FFPE tumor and adjacent normal tissues of another 8 metastatic CRC patients and 8 non-metastatic CRC patients were collected for transcriptome and whole exome sequencing. Mutational burden and signatures were revealed and differentially expressed genes and proteins were analyzed. Molecular Complex Detection was used to build the core network. KEGG and GO pathway enrichment analysis were performed. IHC staining against p-RPS6 and subsequent quantification were performed on human samples.</p><p><strong>Results: </strong>We identified 53,917 SNPs by WES with a median of 1154 variants per sample and 23.08 mutations per megabase (Mb). We observed the mutation burdens were similar between mCRC tumor and nmCRC tumor tissues (p = 0.57), as well as the mutation frequencies of HRR and MMR related genes. All mCRC samples were affected by RTK-RAS, NOTCH and WNT pathway mutations. We constructed a 16-hub-gene network in mCRC which was characterized by dis-modulation of cell adhesion (SELE, SELL and SELP) and immune exhaustion (CXCR2, CCR7, CXCR1, CXCL13, CCL7, CCL19, CXCL11 and CD19) in mCRC tumor microenvironment. We detected 22 differentially expressed proteins, 54 phosphorylated proteins and 6 tyrosine-phosphorylated proteins between mCRC and nmCRC tumors. Phosphorylated RPS6 (p-RPS6) was the most differentially expressed protein between mCRC and nmCRC tumor tissues, which was found to be positively correlated with EMT proteins and poor prognosis in CRC. The IHC staining against p-RPS6 on human samples supported the strong expression in mCRC tumor samples.</p><p><strong>Conclusions: </strong>We identified the key transcriptome network in mCRC and confirmed the important role for RPS6 phosphorylation in mCRC. Our study suggested that the features of mCRC tumors were not driven by gene mutations. We revealed the EMT feature and immune exhaustion of the mCRC tumor microenvironment.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"300"},"PeriodicalIF":6.0,"publicationDate":"2025-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12329991/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144793554","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":"Unlocking the secret of glioblastoma multiforme: the role of lactylation in tumor progression, drug resistance and immune microenvironment.","authors":"Yifei Xiao, Ruipeng Zheng, Fengjun Lv, Guang Yang, Haitao Ge, Mingchun Yang, Kan Wang, Yu Cheng","doi":"10.1186/s12935-025-03933-5","DOIUrl":"10.1186/s12935-025-03933-5","url":null,"abstract":"<p><strong>Background: </strong>Glioblastoma multiforme (GBM), the most prevalent and lethal type of brain cancer, is characterized by a poor prognosis despite advancements in comprehensive treatments, including surgery, chemotherapy, and radiotherapy. Lactylation, an emerging epigenetic modification, has been shown to influence the biological behavior of tumor cells; however, its role in GBM remains to be further elucidated.</p><p><strong>Methods: </strong>In this study, we analyzed the relationship between lactylation-related genes (LRGs) and malignant biological behavior, temozolomide resistance, and the immune microenvironment of GBM using scRNA-seq data from public databases. Subsequently, we identified temozolomide-resistant lactylation-related genes (TMZR-LRGs) through differential gene expression analysis. Based on these genes, we proceeded to classify GBM subtypes and establish a risk prediction model to assess patient prognosis and treatment response. Finally, we validated the impact of lactylation on TMZ resistance and malignant biological behavior of GBM both in vivo and in vitro by knocking out UBE2E1 to increase cellular lactylation levels.</p><p><strong>Result: </strong>ScRNA-seq analysis and in vivo and in vitro experiments both demonstrated that lactylation was significantly up-regulated in GBM cells. In the GBM subtype, MES-like cells have the highest lactylation level. Furthermore, an increase in lactylation levels enhanced the malignant proliferation and temozolomide resistance of GBM cells. The risk model based on TMZR-LRGs effectively predicted the prognosis and immune characteristics of GBM patients and had the potential to accurately identify targeted therapeutic drugs for GBM.</p><p><strong>Conclusion: </strong>Lactylation is critical for malignant progression, temozolomide resistance and the establishment of an immunosuppressive microenvironment of GBM. The risk model based on lactylation-related genes is an effective tool for assessing the prognosis and treatment response of GBM patients. LRGs have potential as therapeutic targets for GBM, providing a new direction for improving patient outcomes.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"299"},"PeriodicalIF":6.0,"publicationDate":"2025-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12330052/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144793556","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: LncRNA HAND2-AS1 exerts anti-oncogenic effects on bladder cancer via restoration of RARB as a sponge of microRNA-146.","authors":"Liping Shan, Wei Liu, Yunhong Zhan","doi":"10.1186/s12935-025-03936-2","DOIUrl":"10.1186/s12935-025-03936-2","url":null,"abstract":"","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"298"},"PeriodicalIF":6.0,"publicationDate":"2025-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12330169/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144793555","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":"Investigating the potential role of miR-451a as a tumor suppressor in immunogenic cell death induction and dendritic cell maturation in colorectal cancer cell lines.","authors":"Mahdieh Azizi, Alireza Andalib, Marzieh Rezaei","doi":"10.1186/s12935-025-03919-3","DOIUrl":"10.1186/s12935-025-03919-3","url":null,"abstract":"<p><strong>Background: </strong>Colorectal cancer (CRC) remains a leading cause of cancer-related mortality, as conventional therapies are frequently hampered by treatment resistance and the presence of an immunosuppressive tumor microenvironment (TME). Immunotherapy, particularly strategies based on immunogenic cell death (ICD) induction can activate the TME by enhancing tumor immunogenicity and promoting T cell infiltration, potentially improving the efficacy of cancer immunotherapies in CRC. This study investigates the potential of miR-451a as a tumor suppressor in the release of ICD associated damage-associated molecular patterns in CRC cell lines and maturation of dendritic cells (DCs).</p><p><strong>Methods: </strong>Human CRC cell lines (SW48, SW1116, SW480, and Caco-2) were treated with oxaliplatin alone or transfected with the hsa-miR-451a mimic, scrambled miRNA, or a combination of the hsa-miR-451a mimic and oxaliplatin for 48 h. Cell viability was measured using MTT assays, and apoptosis was assessed through annexin V and PI staining. Flow cytometry was employed to evaluate calreticulin (CRT) levels on the cell surface and to analyze the percentages of CD11c + CD86 + CD80 + mature DCs. Additionally, ATP levels were quantified using a luminescence assay, and HMGB1 levels were measured by ELISA.</p><p><strong>Results: </strong>Our results demonstrated that the overexpression of miR-451a significantly increased apoptosis and CRT surface exposure in all four CRC cell lines, like the effects observed with oxaliplatin, when compared to both the control and scrambled miRNA groups (P < 0.05, P < 0.01, P < 0.001, and P < 0.0001). However, the combination of miR-451a with oxaliplatin did not yield synergistic effects across all cell lines. Additionally, the ability of miR-451a to increase extracellular ATP and HMGB1 levels, as well as its effect on DC maturation, varied among cell lines.</p><p><strong>Conclusions: </strong>The findings of this study presents novel insights into the potential role of miR-451a as a tumor-suppressive agent in CRC. By examining its effect on ICD across four different CRC cell lines, we provide a comprehensive analysis of its impact on both tumor cells and the immune system. Our results suggest that miR-451a induce certain characteristics of the ICD response, which vary depending on the cellular context.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"297"},"PeriodicalIF":6.0,"publicationDate":"2025-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12329872/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144793553","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":"Role of m6A RNA methylation regulators in pancreatic cancer: interactions and potential implications.","authors":"Li Liao, Xiaoqiang Xu, Yu Cao, Kezhong Tang, Qiaoping Xu","doi":"10.1186/s12935-025-03922-8","DOIUrl":"10.1186/s12935-025-03922-8","url":null,"abstract":"<p><p>Pancreatic cancer (PC) is a highly invasive malignant tumor associated with significant mortality rates, primarily due to challenges in early diagnosis, high invasiveness, and pronounced drug resistance. In recent years, N6-methyladenosine (m6A), one of the most abundant RNA modifications in eukaryotic cells, has been shown to play a critical role in various RNA processes, including alternative splicing, maturation, stability, translation and degradation. m6A is dynamically and reversibly regulated by its methyltransferases, demethylases and m6A-binding proteins, which have been reported to significantly influence the development and progression of various cancers, including PC. We review the latest advancements in m6A regulators and their roles in PC, and introduce the mechanism and signaling pathways of m6A factors affecting PC occurrence and development. Furthermore, we summarize the potential applications of m6A regulators in improving drug resistance and immunotherapy efficacy, as well as the therapeutic promise of small-molecule inhibitors targeting m6A-related proteins, to provide innovative methods and strategies for the diagnosis and treatment of pancreatic cancer.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"292"},"PeriodicalIF":6.0,"publicationDate":"2025-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12320332/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144783574","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":"Very long-chain fatty acids accumulate in breast cancer tissue and serum.","authors":"Alicja Pakiet, Michalina Ciosek, Oliwia Lange, Katarzyna Duzowska, Agata Janczy, Małgorzata Kapusta, Yelyzaveta Razghonova, Marcin Ekman, Anna Abacajew-Chmyłko, Paweł Kabata, Adriana Mika","doi":"10.1186/s12935-025-03928-2","DOIUrl":"10.1186/s12935-025-03928-2","url":null,"abstract":"<p><strong>Background: </strong>Breast cancer (BC) remains one of the most common cancers with relatively high mortality and is associated with alterations in fatty acid (FA) metabolism. While typical FAs have been extensively studied, there is increasing evidence for a potential role of very long chain fatty acids (VLCFAs) in cancer growth and progression.</p><p><strong>Methods: </strong>This study involved 54 BC patients from whom samples of malignant tumor, normal fibroglandular tissue, and breast adipose tissue were collected. Their FA content was analyzed by gas chromatography-mass spectrometry. The expression of fatty acid elongases (ELOVLs) and FA-transporting proteins was analyzed in the tissues by RT-PCR and immunofluorescence.</p><p><strong>Results: </strong>Higher levels of saturated and monounsaturated VLCFAs were found in BC tissues compared to normal tissues (p < 0.001) and in patients' blood compared to healthy controls blood (p < 0.001). However, the level of VLCFAs was lower in BC adipose tissue compared to healthy control adipose tissue (p < 0.001). Interestingly, there were no obvious differences in ELOVL1 mRNA or protein levels between normal and cancer tissues.</p><p><strong>Conclusions: </strong>Elevated levels of VLCFAs in BC tissue are the result of lipid uptake from outside the tumor rather than in situ synthesis.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"296"},"PeriodicalIF":6.0,"publicationDate":"2025-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12320370/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144783575","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":"Promotion of the invasion and metastasis of breast cancer by B7-H3 through CCR5High tumor-associated macrophages.","authors":"Tiantian Dai, Zhihua Xu, Yadi Li, Mengni Wu, Yue Qiu, ZhuJun Chao, Renhai Jiang, Yan Chen, Linlin Lu","doi":"10.1186/s12935-025-03932-6","DOIUrl":"10.1186/s12935-025-03932-6","url":null,"abstract":"<p><p>Breast cancer (BC) ranks first in morbidity and second in mortality in all female cancers, and previous studies support the contribution of tumor-associated macrophages (TAMs) to cancer progression. B7-H3 is aberrantly expressed in a variety of solid cancers, and may also promote cancer progression, but its function is still yet to be known. In this study, the importance of B7-H3 in BC pathogenesis was investigated through TAM. The expression of B7-H3 and CCR5 on macrophages/monocytes was first detected in 135 human BC tissues and peripheral blood by flow cytometry. In the tumor microenvironment, the expression of B7-H3 on TAM was positively correlated with CCR5 levels on TAM. Clinical analysis indicated that CCR5^high TAM was significantly correlated with the size of tumors (T) (P = 0 .011) and E-cadherin (P < 0.0001). In vitro, knockdown of B7-H3 reduced the expression of CCL3/4 on a cell line of monocytes THP-1. Further studies showed that B7-H3 could recruit TAMs through the CCL3/4-CCR5 axis, and that CCR5^highTAM recruited in the tumor microenvironment could enhance BC migration and invasion. In addition, B7-H3 and CCR5 can facilitate the EMT process through the MAPK/ERK and NF-ΚB pathways. In conclusion, it is speculated that B7-H3 may regulate CCR5^high TAMs through the CCL3/4-CCR5 axis, thereby promoting BC migration and invasion.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"293"},"PeriodicalIF":6.0,"publicationDate":"2025-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12320281/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144783573","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}