Carcinogenesis最新文献_第6页

Retraction of: selective killing of human breast cancer cells by the styryl lactone (R)-goniothalamin is mediated by glutathione conjugation, induction of oxidative stress and marked reactivation of the R175H mutant p53 protein. styryl内酯(R)-goniothalamin对人乳腺癌细胞选择性杀伤的撤回是通过谷胱甘肽偶联、诱导氧化应激和R175H突变体p53蛋白的显著再激活介导的。

IF 2.9 3区医学

Carcinogenesis Pub Date : 2025-12-26 DOI: 10.1093/carcin/bgag009

引用次数: 0

MSH2 prevents liver tumorigenesis by regulating cell cycle checkpoints under chronic inflammation. MSH2通过调节慢性炎症下的细胞周期检查点来预防肝脏肿瘤发生。

IF 3.8 3区医学

Carcinogenesis Pub Date : 2025-12-26 DOI: 10.1093/carcin/bgag005

Shigeharu Nakano, Atsushi Takai, Eriko Iguchi, Yosuke Fujii, Haruka Amino, Masayuki Ueno, Takahiko Ito, Mari Teramura, Masako Mishima, Ken Kumagai, Tadashi Inuzuka, Haruhiko Takeda, Yuji Eso, Takahiro Shimizu, Takahisa Maruno, Hiroshi Seno

{"title":"MSH2 prevents liver tumorigenesis by regulating cell cycle checkpoints under chronic inflammation.","authors":"Shigeharu Nakano, Atsushi Takai, Eriko Iguchi, Yosuke Fujii, Haruka Amino, Masayuki Ueno, Takahiko Ito, Mari Teramura, Masako Mishima, Ken Kumagai, Tadashi Inuzuka, Haruhiko Takeda, Yuji Eso, Takahiro Shimizu, Takahisa Maruno, Hiroshi Seno","doi":"10.1093/carcin/bgag005","DOIUrl":"10.1093/carcin/bgag005","url":null,"abstract":"The DNA mismatch repair (MMR) system plays a critical role in maintaining genomic integrity and preventing tumorigenesis. Although MutS homolog 2 (MSH2) is a key component of the MMR system and is dysregulated in human hepatocellular carcinoma (HCC), the molecular mechanism of MSH2 in the process of HCC development under chronic inflammatory conditions remains unclear. To investigate the function of MSH2 in inflammation-associated hepatocarcinogenesis, we treated hepatocyte-specific Msh2-knockout (Msh2 KO) mice with 0.02% thioacetamide for 30 weeks to induce chronic liver inflammation and examined their phenotype. Msh2 KO mice exhibited higher liver tumor incidence than wild-type mice, with no major differences in inflammation or fibrosis. Whole-exome sequencing analysis revealed that genetic alterations with defective MMR-associated signatures were increased in Msh2 KO tumors, though no common cancer driver genes were identified. Transcriptome analysis revealed enrichment of cell cycle-related gene sets, including the G2M checkpoint and E2F targets. Functional assays further demonstrated that MSH2 downregulation impaired ATM-CHK2-mediated DNA damage response and promoted cell cycle acceleration. MSH2 exerts its tumor-suppressive effects in hepatocytes not only through canonical MMR but also by regulating the cell cycle via the ATM-CHK2 axis.","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":" ","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-12-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146084466","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

LncRNA-encoded peptide LRRC75A-AS1-ORF3 suppresses anti-tumor immunity in colorectal cancer through mitophagy-mediated attenuation of cGAS-STING signaling. lncrna编码的肽LRRC75A-AS1-ORF3通过线粒体自噬介导的cGAS-STING信号的衰减抑制结直肠癌的抗肿瘤免疫。

IF 3.8 3区医学

Carcinogenesis Pub Date : 2025-12-26 DOI: 10.1093/carcin/bgaf092

Qi Wu, Zhun Li, Xinxin He, Shuhui Yu, Mengrou Zhang, Hui Mo, Saiqi He, Jianming Li, Wen Ni

{"title":"LncRNA-encoded peptide LRRC75A-AS1-ORF3 suppresses anti-tumor immunity in colorectal cancer through mitophagy-mediated attenuation of cGAS-STING signaling.","authors":"Qi Wu, Zhun Li, Xinxin He, Shuhui Yu, Mengrou Zhang, Hui Mo, Saiqi He, Jianming Li, Wen Ni","doi":"10.1093/carcin/bgaf092","DOIUrl":"10.1093/carcin/bgaf092","url":null,"abstract":"Long non-coding RNAs (lncRNAs) serve as pivotal regulators of diverse physiological activities through their interactions with different biomolecules, and their aberrant expression frequently contributes to tumorigenesis and malignant progression. Emerging evidence has demonstrated that certain lncRNAs contain open reading frames that can generate useful short peptides, which influence cancer-related physiological and pathological pathways via diverse mechanisms. In this research, we identified that the lncRNA LRRC75A-AS1 encodes a conserved peptide consisting of 102 amino acids, designated as LRRC75A-AS1-ORF3. Notably, this peptide acts independently of the non-coding RNA itself to suppress anti-tumor immune responses and promote colorectal cancer progression. Mechanistically, LRRC75A-AS1-ORF3 is localized in the mitochondria, where it induces mitophagy, thereby eliminating cytosolic mitochondrial DNA (mtDNA) and downregulating the cGAS-STING signaling pathway. Our findings reveal a previously uncharacterized mechanism by which LRRC75A-AS1-ORF3 impairs anti-tumor immunity, thereby presenting a novel immunotherapeutic target for colorectal cancer treatment.","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":" ","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-12-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145780494","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

microRNA involvement in human cancer. microRNA在人类癌症中的作用

IF 3.8 3区医学

Carcinogenesis Pub Date : 2025-12-26 DOI: 10.1093/carcin/bgaf066

Marilena V Iorio, Carlo M Croce

{"title":"microRNA involvement in human cancer.","authors":"Marilena V Iorio, Carlo M Croce","doi":"10.1093/carcin/bgaf066","DOIUrl":"10.1093/carcin/bgaf066","url":null,"abstract":"When, ∼20 years ago, investigators first determined that components of the genome considered nonfunctional had, in fact, gene regulatory capacity, they probably had no idea of their potential in controlling cell fate and were forced to revise and somehow reorganize their view of the molecular biology. Indeed, it is currently well documented how a class of small non-coding RNAs, microRNAs, are conserved among the species, expressed in different tissues and cell types and involved in almost every biological process, including cell cycle, growth, apoptosis, differentiation and stress response, exerting a finely tuned regulation of gene expression by targeting multiple molecules. As a consequence of the widespread range of processes they are able to influence, it is not surprising that miRNA deregulation is a hallmark of several pathological conditions, including cancer. Indeed, the aberrant expression of these tiny molecules in human tumors is not just a casual association, but they can exert a causal role, as oncogenes or tumor suppressors, in every step of tumor development, from occurrence to progression. An increasing body of evidence has indeed proved the importance of miRNAs in cancer, suggesting their possible use as diagnostic, prognostic and predictive biomarkers and leading to exploit miRNA-based anticancer therapies, either alone or in combination with current targeted therapies, with the goal to improve disease response and increase cure rates. Here, we review our current knowledge about miRNA involvement in cancer.","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":"47 1","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-12-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13439581/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146156116","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}

引用次数: 0

Expression of Concern: The promoting effects of hsa_circ_0050102 in pancreatic cancer and the molecular mechanism by targeting miR-1182/NPSR1. 关注表达：hsa_circ_0050102在胰腺癌中的促进作用及其靶向miR-1182/NPSR1的分子机制。

IF 2.9 3区医学

Carcinogenesis Pub Date : 2025-12-26 DOI: 10.1093/carcin/bgag010

引用次数: 0

Functional significance of the aryl hydrocarbon receptor in oncogenic signaling pathways. 芳烃受体在致癌信号通路中的功能意义。

IF 3.8 3区医学

Carcinogenesis Pub Date : 2025-12-26 DOI: 10.1093/carcin/bgaf068

Blake M Arciga, Ananya Katepalli, Nagabhishek Sirpu Natesh, Emma Teixeiro, Jussuf T Kaifi, Satyanarayana Rachagani

{"title":"Functional significance of the aryl hydrocarbon receptor in oncogenic signaling pathways.","authors":"Blake M Arciga, Ananya Katepalli, Nagabhishek Sirpu Natesh, Emma Teixeiro, Jussuf T Kaifi, Satyanarayana Rachagani","doi":"10.1093/carcin/bgaf068","DOIUrl":"10.1093/carcin/bgaf068","url":null,"abstract":"The aryl hydrocarbon receptor (AhR) is a ubiquitously expressed, ligand-activated transcription factor which has been extensively studied for its role in mediating the toxic effects of several common environmental pollutants. However, more recent findings associating AhR with carcinogenesis and tumor progression have expanded the scope of AhR research and established the preclinical significance of AhR as a possible target for cancer therapy. In this review, the current knowledge of the role of AhR in cancer will be discussed, and evidence from an array of experimental cancer and immune models will be presented. It has been observed that AhR potentiates oncogenic mutations through induction of genetic damage and transactivates EGFR to promote proproliferative signaling along the classical Ras/Raf/MAPK and PI3K/Akt pathways. Furthermore, AhR downregulates E-cadherin via multiple axes to facilitate epithelial-to-mesenchymal transition and contributes to a shift of the tumor immune microenvironment to a predominantly regulatory milieu. The sheer versatility of AhR as a protumor factor should provide sufficient grounds for further investigation of the persisting question of whether targeting AhR can disrupt tumor progression in vivo.","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":"47 1","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-12-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13017131/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147369150","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}

引用次数: 0

Retraction and replacement of: microRNA involvement in human cancer. microRNA在人类癌症中的作用。

IF 3.8 3区医学

Carcinogenesis Pub Date : 2025-12-26 DOI: 10.1093/carcin/bgaf065

引用次数: 0

Retraction of: Increased expression of the MGMT repair protein mediated by cysteine prodrugs and chemopreventative natural products in human lymphocytes and tumor cell lines. 收缩：半胱氨酸前药和化学预防天然产物介导的MGMT修复蛋白在人淋巴细胞和肿瘤细胞系中的表达增加。

IF 2.9 3区医学

Carcinogenesis Pub Date : 2025-12-26 DOI: 10.1093/carcin/bgag004

引用次数: 0

A dual approach to glioblastoma treatment with epigenetic reprogramming and neurogenetic modulation. 用表观遗传重编程和神经遗传调节双重方法治疗胶质母细胞瘤。

IF 3.8 3区医学

Carcinogenesis Pub Date : 2025-12-26 DOI: 10.1093/carcin/bgag008

Mustafa Eren Yuncu, Berra Bilgin, Derin Avci, Ali Karadag, Fusun Ozer, Cigir Biray Avci

{"title":"A dual approach to glioblastoma treatment with epigenetic reprogramming and neurogenetic modulation.","authors":"Mustafa Eren Yuncu, Berra Bilgin, Derin Avci, Ali Karadag, Fusun Ozer, Cigir Biray Avci","doi":"10.1093/carcin/bgag008","DOIUrl":"10.1093/carcin/bgag008","url":null,"abstract":"Glioblastoma is a highly aggressive primary brain tumour marked by extensive genomic and epigenomic alterations, cellular heterogeneity, and therapeutic resistance. Despite maximal surgical resection followed by chemoradiotherapy, median survival remains approximately 15 months, reflecting the tumour's invasive behaviour and adaptability. Advances in molecular oncology have revealed two promising therapeutic directions: epigenetic reprogramming and neurogenetic modulation. Glioblastoma exhibits widespread epigenetic dysregulation that disrupts transcriptional control, enhances cellular plasticity, and drives tumour progression. Concurrently, glioma cells aberrantly reactivate developmental programmes, acquiring neural stem cell-like states governed by transcription factors and signalling networks such as SOX2, OLIG2, Notch, and Wnt. These pathways collectively sustain stemness, lineage mimicry, and therapy resistance. This review proposes a focused conceptual framework centred on epigenetic and neurogenetic modulation as two core regulatory layers shaping glioblastoma plasticity and adaptive resistance. We highlight how DNA methylation, histone modifications, and chromatin remodelling contribute to transcriptional dysregulation, and how neurodevelopmental signalling reinforces malignant plasticity. Emerging preclinical and clinical studies combining epigenetic inhibitors with differentiation- or reprogramming-based therapies are discussed. By uniting mechanistic insights from chromatin biology, neurodevelopment, and cancer therapeutics, this integrative conceptual framework offers a structured lens for targeting key vulnerabilities underlying glioblastoma plasticity. The integration of these complementary strategies offers potential to enhance therapeutic responsiveness and improve disease management in this devastating malignancy.","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":" ","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-12-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147281883","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

High-glucose environment reduces keratinocyte migration and proliferation via inhibition of SOX2: implications on UV-induced skin tumors in patients with diabetes. 高糖环境通过抑制SOX2降低角化细胞的迁移和增殖：对糖尿病患者紫外线诱导的皮肤肿瘤的影响

IF 3.8 3区医学

Carcinogenesis Pub Date : 2025-12-26 DOI: 10.1093/carcin/bgag013

Ting-Ting Yang, Shu-Mei Huang, Yu-Ting Peng, Cheng-Che E Lan

{"title":"High-glucose environment reduces keratinocyte migration and proliferation via inhibition of SOX2: implications on UV-induced skin tumors in patients with diabetes.","authors":"Ting-Ting Yang, Shu-Mei Huang, Yu-Ting Peng, Cheng-Che E Lan","doi":"10.1093/carcin/bgag013","DOIUrl":"10.1093/carcin/bgag013","url":null,"abstract":"While the effect of hyperglycemia on cutaneous wound healing is well recognized, the impact of high-glucose (HG) environment on UVB-induced skin tumor formation remains inconclusive. Similar to impaired wound healing, skin tumor formation involves keratinocyte proliferation and migration. Intriguingly, SOX2 has been recognized to play an important role in both wound healing and UVB-induced skin tumor formation by modulating cell proliferation and migration. As hyperglycemia results in impaired cutaneous wound healing, we hypothesized that the HG environment also impacts UVB-induced tumor formation of the skin. This study aimed to explore the effects of HG environment on epidermal keratinocytes, focusing on the impact of UVB-induced cell proliferation and migration via SOX2 expression. In cultured keratinocytes, HG-cultivated keratinocytes showed reduced SOX2 levels compared to control with or without UVB treatment. SOX2 regulates keratinocyte migration and proliferation via modulation of AKT phosphorylation. Additionally, O-linked-N-acetylglucosamine glycosylation contributed to reduced SOX2 levels in HG-cultivated keratinocytes. Animal studies demonstrated that diabetic mice skin has significantly less UVB-induced tumor formation, epidermal thickening, SOX2, and pAKT expression than the control mice; mutant p53 expression was also lower in diabetic mice but did not reach statistical significance compared to control. In conclusion, HG environment reduces UVB-induced keratinocyte proliferation and migration, in association with decreased SOX2 expression and downstream AKT signaling. The current findings provide novel insights regarding UVB-induced skin tumor formation of skin in patients with diabetes.","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":" ","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-12-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147321386","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0