International Journal of Biological Sciences最新文献

Acute Exposure to Cadmium Triggers NCOA4-Mediated Ferritinophagy and Ferroptosis in Never-Smokers Oral Cancer Cells. 急性镉暴露引发非吸烟者口腔癌细胞ncoa4介导的铁蛋白吞噬和铁凋亡。

IF 8.2 2区生物学

International Journal of Biological Sciences Pub Date : 2025-06-20 eCollection Date: 2025-01-01 DOI: 10.7150/ijbs.111228

Lavinia Petriaggi, Emanuele Giorgio, Stefania Bulotta, Alessandro Antonelli, Sonia Bonacci, Marialaura Frisina, Antonio Procopio, Licia Elvira Prestagiacomo, Annarita Giuliano, Marco Gaspari, Gianluca Santamaria, Giorgia Federico, Cristiana Galeano, Giuseppe Natali, Amerigo Giudice, Francesco Costanzo, Anna Martina Battaglia, Flavia Biamonte

{"title":"Acute Exposure to Cadmium Triggers NCOA4-Mediated Ferritinophagy and Ferroptosis in Never-Smokers Oral Cancer Cells.","authors":"Lavinia Petriaggi, Emanuele Giorgio, Stefania Bulotta, Alessandro Antonelli, Sonia Bonacci, Marialaura Frisina, Antonio Procopio, Licia Elvira Prestagiacomo, Annarita Giuliano, Marco Gaspari, Gianluca Santamaria, Giorgia Federico, Cristiana Galeano, Giuseppe Natali, Amerigo Giudice, Francesco Costanzo, Anna Martina Battaglia, Flavia Biamonte","doi":"10.7150/ijbs.111228","DOIUrl":"10.7150/ijbs.111228","url":null,"abstract":"Cadmium (Cd), a carcinogenic component of tobacco, is a recognized risk factor for oral squamous cell carcinoma (OSCC). However, the molecular mechanisms underlying Cd-induced cytotoxicity in OSCC remain largely undefined. Here, we demonstrate that acute Cd exposure triggers ferroptosis in CAL27 OSCC cells derived from never-smokers, but not in SCC154 cells derived from smokers. Mechanistically, Cd outcompetes Fe, causing early iron depletion and activating the nuclear receptor coactivator 4 (NCOA4)-mediated ferritinophagy. This process enhances the labile iron pool, promotes mitochondrial reactive oxygen species (ROS) generation, lipid peroxidation, and ferroptotic cell death. Notably, iron supplementation rescues CAL27 cells from Cd-induced damage, while exacerbating iron deficiency through transferrin receptor CD71 silencing amplifies cytotoxicity. Conversely, OSCC cells from smokers exhibit resistance to Cd toxicity, likely due to the overexpression of metallothionein 2A (MT2A), a heavy metal detoxification protein. Collectively, this study provides the evidence that ferritinophagy may act as a critical upstream driver of Cd-induced ferroptosis in OSCC cells derived from never-smokers, paving the way for potential ferroptosis-targeted therapeutic strategies in Cd-associated malignancies.","PeriodicalId":13762,"journal":{"name":"International Journal of Biological Sciences","volume":"21 9","pages":"4131-4152"},"PeriodicalIF":8.2,"publicationDate":"2025-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12223766/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144559967","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Enhancing CAR-T Cell Metabolic Fitness and Memory Phenotype for Improved Efficacy against Hepatocellular Carcinoma. 增强CAR-T细胞代谢适应性和记忆表型以提高抗肝细胞癌的疗效。

IF 8.2 2区生物学

International Journal of Biological Sciences Pub Date : 2025-06-20 eCollection Date: 2025-01-01 DOI: 10.7150/ijbs.110406

Jinqi You, Xinyi Yang, Jingjing Zhao, Hao Chen, Yan Tang, Dijun Ouyang, Yuanyuan Liu, Yan Wang, Songzuo Xie, Yuanyuan Chen, Jinghao Liao, Tong Xiang, Jianchuan Xia, Chaopin Yang, Desheng Weng

{"title":"Enhancing CAR-T Cell Metabolic Fitness and Memory Phenotype for Improved Efficacy against Hepatocellular Carcinoma.","authors":"Jinqi You, Xinyi Yang, Jingjing Zhao, Hao Chen, Yan Tang, Dijun Ouyang, Yuanyuan Liu, Yan Wang, Songzuo Xie, Yuanyuan Chen, Jinghao Liao, Tong Xiang, Jianchuan Xia, Chaopin Yang, Desheng Weng","doi":"10.7150/ijbs.110406","DOIUrl":"10.7150/ijbs.110406","url":null,"abstract":"The persistence of chimeric antigen receptor (CAR) T cells in the tumor microenvironment limits their antitumor effects against solid tumors. Many studies have reported that the in vitro phenotype and metabolism of CAR-T cells correlates with their in vivo antitumor activity. Herein, we constructed PD-1 scFv-secreting and CD133-specific CAR-T (referred to as CAR-T) cells based on our previous work. We found that suitable concentration metformin-treated CAR-T (mCAR-T) cells exhibited an increased memory phenotype and demonstrated stronger and faster antitumor abilities with a reduced exhaustion phenotype. Using RNA sequencing, transmission electron microscope, and metabolic analysis, we discovered enhanced mitochondrial biogenesis and metabolism in CAR-T cells treated with 10 μM metformin, is associated with increased peroxisome proliferator-activated receptor gamma coactivator-1alpha (PGC-1α) expression, promotion of signal transducer and activator of transcription (STAT)3 and inhibition of STAT5 phosphorylation. This resulted in enhanced antitumor effects of mCAR-T cells in both subcutaneous and orthotopic xenograft models. Importantly, in some relapsed hepatocellular carcinoma (HCC) patients, high CD133 expression was observed in their paired primary or metastatic tumor sections. Our study revealed that enhancing metabolic fitness and central memory by in vitro metformin treatment is an effective strategy to improve the efficacy of CAR-T cell therapy, potentially benefiting some relapsed HCC patients.","PeriodicalId":13762,"journal":{"name":"International Journal of Biological Sciences","volume":"21 9","pages":"4231-4251"},"PeriodicalIF":8.2,"publicationDate":"2025-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12224003/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144560069","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Cancer-associated Fibroblast-like Cells Promote Osteosarcoma Metastasis by Upregulation of Phosphoserine Aminotransferase 1 and Activation of the mTOR/S6K Pathway. 癌症相关成纤维细胞样细胞通过上调磷酸丝氨酸转氨酶1和激活mTOR/S6K通路促进骨肉瘤转移

IF 8.2 2区生物学

International Journal of Biological Sciences Pub Date : 2025-06-20 eCollection Date: 2025-01-01 DOI: 10.7150/ijbs.109169

Liwen Feng, Guangqin Xiao, Yuting Chen, Ting Ye, Li Fan, Yuxiu Xie, Ting Mei, Lei Wang, Jingjing Ge, Chengzhi Ye, Jing Chen

{"title":"Cancer-associated Fibroblast-like Cells Promote Osteosarcoma Metastasis by Upregulation of Phosphoserine Aminotransferase 1 and Activation of the mTOR/S6K Pathway.","authors":"Liwen Feng, Guangqin Xiao, Yuting Chen, Ting Ye, Li Fan, Yuxiu Xie, Ting Mei, Lei Wang, Jingjing Ge, Chengzhi Ye, Jing Chen","doi":"10.7150/ijbs.109169","DOIUrl":"10.7150/ijbs.109169","url":null,"abstract":"Metastasis remains a major obstacle limiting the survival of patients with osteosarcoma (OS). Cross-talk between cancer-associated fibroblasts (CAFs) and OS cells has been found to facilitate metastasis, although the effects of CAFs on OS cell metabolism are poorly understood. Here, conditioned medium from OS cells was used to activate CAF-like cells, which was found to promote OS migration and the epithelial-mesenchymal transition. Metabolomics analysis showed that treatment of OS cells with CAFs-conditioned medium significantly altered the levels of phosphoserine aminotransferase 1 (PSAT1), a key serine synthase. CAF-induced OS cell migration was inhibited by PSAT1 knockdown by siRNA, and PSAT1 was found to promote migration through the PI3K/mTOR/S6K pathway. The influence of CAFs on OS metastasis was blocked by PSAT1 knockdown and mTOR inhibitors in vitro and in vivo. In conclusion, the findings suggest that PSAT1 and the mTOR/S6K pathway have the potential as targets for preventing OS metastasis.","PeriodicalId":13762,"journal":{"name":"International Journal of Biological Sciences","volume":"21 9","pages":"4153-4171"},"PeriodicalIF":8.2,"publicationDate":"2025-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12223780/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144560066","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

SESN2 inhibits tubular exosome secretion and diabetic kidney disease progression by restoring the autophagy‒lysosome pathway. SESN2通过恢复自噬-溶酶体途径抑制小管外泌体分泌和糖尿病肾病进展。

IF 8.2 2区生物学

International Journal of Biological Sciences Pub Date : 2025-06-20 eCollection Date: 2025-01-01 DOI: 10.7150/ijbs.109799

Zongji Zheng, Jiaqi Chen, Xiaoquan Xue, Xiaoqin Ma, Shuting Zhang, Ming Wang, Yaoming Xue, Yijie Jia

{"title":"SESN2 inhibits tubular exosome secretion and diabetic kidney disease progression by restoring the autophagy‒lysosome pathway.","authors":"Zongji Zheng, Jiaqi Chen, Xiaoquan Xue, Xiaoqin Ma, Shuting Zhang, Ming Wang, Yaoming Xue, Yijie Jia","doi":"10.7150/ijbs.109799","DOIUrl":"10.7150/ijbs.109799","url":null,"abstract":"During diabetic kidney disease (DKD), tubulointerstitial fibrosis persists, although several methods have been applied to reduce albuminuria levels. In this research, we found that bovine serum albumin (BSA)-induced renal tubular cell injury could also spread to normal tubular cells through exosomes, which may explain why tubulointerstitial fibrosis persists. Our previous studies revealed that SESN2 overexpression alleviates tubular dysfunction. In this study, we showed that SESN2 overexpression in donor HK2 cells interrupted this \"doom loop\" and confirmed that SESN2 may mediate this process by reducing exosome secretion. By using RNA-seq and IP-MS, we found that SESN2 could inhibit BSA-induced Rab-7a ubiquitination, thus promoting autophagosome and lysosome fusion and accelerating MVB degradation. We also showed that SESN2 promotes the nuclear translocation of TFEB through the mTOR pathway, thus further alleviating lysosomal function and promoting MVB degradation. We also found that SESN2 not only slowed DKD progression but also promoted renal tubular cell secretion of protective exosomes, which also slowed DKD progression. In conclusion, SESN2 can interrupt the progression of albuminuria-induced tubular injury by inhibiting exosome secretion and promoting MVB degradation. Thus, SESN2 may be a new therapeutic target for DKD treatment.","PeriodicalId":13762,"journal":{"name":"International Journal of Biological Sciences","volume":"21 9","pages":"4215-4230"},"PeriodicalIF":8.2,"publicationDate":"2025-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12223778/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144560076","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Decoding the Tumor Microenvironment: Exosome-Mediated Macrophage Polarization and Therapeutic Frontiers. 解码肿瘤微环境：外泌体介导的巨噬细胞极化和治疗前沿。

IF 8.2 2区生物学

International Journal of Biological Sciences Pub Date : 2025-06-20 eCollection Date: 2025-01-01 DOI: 10.7150/ijbs.114222

Yilin Li, Jiaqi You, Zifang Zou, Guanghao Sun, Yuqing Shi, Yanbin Sun, Shun Xu, Xin Zhang

{"title":"Decoding the Tumor Microenvironment: Exosome-Mediated Macrophage Polarization and Therapeutic Frontiers.","authors":"Yilin Li, Jiaqi You, Zifang Zou, Guanghao Sun, Yuqing Shi, Yanbin Sun, Shun Xu, Xin Zhang","doi":"10.7150/ijbs.114222","DOIUrl":"10.7150/ijbs.114222","url":null,"abstract":"The tumor microenvironment (TME) is dynamically shaped by interactions between tumor cells, immune cells, and stromal components. Among these, tumor-associated macrophages (TAMs) play dual roles in tumor progression. Exosomes are key mediators of intercellular communication and are crucial for modulating macrophage polarization. This review systematically summarizes the role of HIF-1α as the central regulator of tumor-derived exosomes under hypoxic conditions. Under endoplasmic reticulum stress (ERS), the STAT3 and PI3K/AKT/mTOR pathways activation is mediated by the inactivation of the Hsp90/Hippo pathway, which induces the expression of LncRNA HMMR-AS1 and specific miRNAs (e.g., miR-1246, let-7a, miR-301a-3p, etc.). Furthermore, the IRE1/PERK pathway regulates exosome secretion by carrying miR-23a-3p and miR-27a-3p or directly delivering PD-L1 protein, thus activating the PI3K/AKT pathway, inhibiting PTEN, and upregulating PD-L1 expression as well as increasing the M2 polarization of macrophages. This study also summarized the important matrices of exosomes' involvement in the interaction between tumor cells and macrophages in different systemic malignant tumors. Moreover, the bidirectional crosstalk between TAM-derived exosomes and other TME components (e.g., CD8+ T cells, fibroblasts) was also evaluated, which indicated their roles in immune evasion and metastasis. Further, engineering strategies, such as receptor-targeted exosomes and short palindromic repeats interference (CRISPRi)-based transcriptional silencing, were also discussed as emerging tools to enhance exosome specificity and therapeutic efficacy. This study proposes a roadmap for translating engineered exosomes into clinical immunotherapy regimens by integrating recent advances in spatial omics and artificial intelligence, and also addresses challenges in exosome isolation, stability, and biosafety.","PeriodicalId":13762,"journal":{"name":"International Journal of Biological Sciences","volume":"21 9","pages":"4187-4214"},"PeriodicalIF":8.2,"publicationDate":"2025-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12223767/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144560068","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Coupling of glucose metabolism with mitophagy via O-GlcNAcylation of PINK1. 通过PINK1的o - glcn酰化，糖代谢与线粒体自噬的偶联。

IF 8.2 2区生物学

International Journal of Biological Sciences Pub Date : 2025-06-20 eCollection Date: 2025-01-01 DOI: 10.7150/ijbs.112672

Zhiwei Xu, Xiangzheng Gao, Dade Rong, Jingyao Wang, Liangliang Gao, Mingzhu Tang, Yiguan Chen, Yichi Zhang, Liming Xie, Liming Wang, Guang Lu, Jia-Hong Lu, Wei Liu, Han-Ming Shen

{"title":"Coupling of glucose metabolism with mitophagy via O-GlcNAcylation of PINK1.","authors":"Zhiwei Xu, Xiangzheng Gao, Dade Rong, Jingyao Wang, Liangliang Gao, Mingzhu Tang, Yiguan Chen, Yichi Zhang, Liming Xie, Liming Wang, Guang Lu, Jia-Hong Lu, Wei Liu, Han-Ming Shen","doi":"10.7150/ijbs.112672","DOIUrl":"10.7150/ijbs.112672","url":null,"abstract":"Mitophagy is a selective form of autophagy for the clearance of damaged and dysfunctional mitochondria via the autophagy-lysosome pathway. As mitochondria are the most important metabolic organelles, the process of mitophagy is tightly regulated by glucose metabolism. At present, it is known that glucose is required for the mitophagy process, while the underlying mechanisms remain to be further elucidated. In this study, we establish a novel regulatory role of glucose metabolism in mitophagy via protein O-GlcNAcylation. First, we found that acute mitochondrial damage enhanced glucose uptake and promoted protein O-GlcNAcylation. Second, we provided evidence that protein O-GlcNAcylation promotes PINK1-Parkin-dependent mitophagy. Next, we attempted to illustrate the molecular mechanisms underlying the regulation of O-GlcNAcylation in mitophagy by focusing on PTEN-induced kinase 1 (PINK1). One important observation is that PINK1 is O-GlcNAcylated upon acute mitochondrial damage, and suppression of O-GlcNAcylation impairs PINK1 protein stability and its phosphorylated ubiquitin, leading to impaired mitophagy. More importantly, we found that glucose metabolism promotes mitophagy via regulating O-GlcNAcylation. Taken together, this study demonstrates a novel regulatory mechanism connecting glucose metabolism with mitophagy via O-GlcNAcylation of PINK1. Therefore, targeting the O-GlcNAcylation may provide new strategies for the modulation of mitophagy and mitophagy-related human diseases.","PeriodicalId":13762,"journal":{"name":"International Journal of Biological Sciences","volume":"21 9","pages":"4252-4269"},"PeriodicalIF":8.2,"publicationDate":"2025-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12224001/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144560067","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

NASP Promotes Triple-negative Breast Cancer Progression and Metastasis by Stabilizing YAP in a USP15-Dependent Way. NASP通过稳定YAP以usp15依赖的方式促进三阴性乳腺癌进展和转移。

IF 8.2 2区生物学

International Journal of Biological Sciences Pub Date : 2025-06-20 eCollection Date: 2025-01-01 DOI: 10.7150/ijbs.99438

Wenfang Zheng, Qifeng Luo, Xuehui Wang, Xiqian Zhou, Danrong Ye, Kaiyao Hua, Lin Fang

{"title":"NASP Promotes Triple-negative Breast Cancer Progression and Metastasis by Stabilizing YAP in a USP15-Dependent Way.","authors":"Wenfang Zheng, Qifeng Luo, Xuehui Wang, Xiqian Zhou, Danrong Ye, Kaiyao Hua, Lin Fang","doi":"10.7150/ijbs.99438","DOIUrl":"10.7150/ijbs.99438","url":null,"abstract":"Triple-negative breast cancer (TNBC) was a subtype of breast cancer with high rate of metastasis and poor prognosis. Thus, it is urgent to explore the underlying mechanism of TNBC metastasis and seek for potential therapeutic targets to improve the prognosis of TNBC patients. Here we reported that nuclear autoantigenic sperm protein (NASP) was highly expressed in TNBC and related to poor prognosis of TNBC patients. NASP acted as an oncogene that promoted the progression and metastasis of TNBC. Mechanistically, high expression of NASP in TNBC was induced by SRSF1-mediated stabilization of NASP mRNA. NASP interacted with USP15 and facilitated its activity, which resulted in the deubiquitylation and stabilization of YAP by erasing K48-linked polyubiquitination. Moreover, in vivo studies validated the role of NASP in stimulating TNBC growth and metastasis. Altogether, NASP promoted TNBC progression and metastasis by stabilizing YAP in a USP15-dependent way. It might provide new insights and potential therapeutic targets for preventing TNBC metastasis and improving the prognosis of TNBC patients.","PeriodicalId":13762,"journal":{"name":"International Journal of Biological Sciences","volume":"21 9","pages":"4172-4186"},"PeriodicalIF":8.2,"publicationDate":"2025-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12223775/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144560073","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Deubiquitylating Enzymes in Hepatocellular Carcinoma. 肝细胞癌中的去泛素化酶。

IF 8.2 2区生物学

International Journal of Biological Sciences Pub Date : 2025-06-20 eCollection Date: 2025-01-01 DOI: 10.7150/ijbs.113193

Xingyu Mi, Qingfeng Li, Guo Long, Yilin Pan, Yulin Xie, Shiqi Lu, Liang Xiao, Jianing Tang, Ledu Zhou

{"title":"Deubiquitylating Enzymes in Hepatocellular Carcinoma.","authors":"Xingyu Mi, Qingfeng Li, Guo Long, Yilin Pan, Yulin Xie, Shiqi Lu, Liang Xiao, Jianing Tang, Ledu Zhou","doi":"10.7150/ijbs.113193","DOIUrl":"10.7150/ijbs.113193","url":null,"abstract":"Ubiquitination is a reversible and dynamic process, precisely regulated by ubiquitin-activating enzymes (E1), ubiquitin-conjugating enzymes (E2), ubiquitin ligases (E3), and deubiquitinating enzymes (DUBs). Dysregulation of DUBs disrupts the dynamic balance of ubiquitination, contributing to the development of various diseases, particularly cancer. An increasing number of studies have identified dysregulation of DUBs in various tumor types and have explored their regulatory mechanisms in these contexts. Hepatocellular carcinoma (HCC), the most common form of liver cancer, is highly malignant and has limited treatment options, necessitating the exploration of additional therapeutic strategies. Current research has identified dysregulation of DUBs in HCC, but their mechanisms of action remain poorly understood. Given the large number of DUB family members, there is significant potential for further investigation. This review summarizes the DUBs associated with HCC, including their structures, functions, and the mechanisms through which they regulate HCC development. Furthermore, we provide a brief overview of the discussed DUBs, aiming to offer new perspectives for future HCC research.","PeriodicalId":13762,"journal":{"name":"International Journal of Biological Sciences","volume":"21 9","pages":"4270-4292"},"PeriodicalIF":8.2,"publicationDate":"2025-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12210126/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144553468","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Erratum: cDCBLD2 mediates sorafenib resistance in hepatocellular carcinoma by sponging miR-345-5p binding to the TOP2A coding sequence: Erratum. 勘误：cDCBLD2通过海绵miR-345-5p结合TOP2A编码序列介导肝细胞癌的索拉非尼耐药：勘误。

IF 8.2 2区生物学

International Journal of Biological Sciences Pub Date : 2025-06-16 eCollection Date: 2025-01-01 DOI: 10.7150/ijbs.113876

YeLing Ruan, TianYi Chen, LongBo Zheng, JingWei Cai, Hu Zhao, YaLi Wang, LiYe Tao, JunJie Xu, Lin Ji, XiuJun Cai

引用次数: 0

Promoter Hyper-methylation of ZNF662 Restrains its Tumor Suppressing Function in Triple-Negative Breast Cancer Through Regulating NGF Signaling Axis. ZNF662启动子超甲基化通过调节NGF信号轴抑制三阴性乳腺癌的抑瘤功能

IF 8.2 2区生物学

International Journal of Biological Sciences Pub Date : 2025-06-12 eCollection Date: 2025-01-01 DOI: 10.7150/ijbs.102940

Renjie Yu, Xi Peng, Zhaobo Cheng, Yue Wu, Huan Rong, Lin Yi, Jing Ran, Chaoqun Deng, Xiangyi Zhou, Ruijie Ming, Ningning Zhang, Xiaoyu Liu, Xiaohua Zeng, Yun Xiao, Xue Wang, Yongzhong Wu, Bo Qin, Tingxiu Xiang

{"title":"Promoter Hyper-methylation of ZNF662 Restrains its Tumor Suppressing Function in Triple-Negative Breast Cancer Through Regulating NGF Signaling Axis.","authors":"Renjie Yu, Xi Peng, Zhaobo Cheng, Yue Wu, Huan Rong, Lin Yi, Jing Ran, Chaoqun Deng, Xiangyi Zhou, Ruijie Ming, Ningning Zhang, Xiaoyu Liu, Xiaohua Zeng, Yun Xiao, Xue Wang, Yongzhong Wu, Bo Qin, Tingxiu Xiang","doi":"10.7150/ijbs.102940","DOIUrl":"10.7150/ijbs.102940","url":null,"abstract":"Triple-negative breast cancer (TNBC) has the highest mortality rate among common cancers in women. Thus, the identification of new therapeutic targets is of major significance. Our study identifies ZNF662 as a novel member of KRAB-containing zinc finger proteins (KRAB-ZFPs) family in TNBC. However, its biological function and potential mechanisms in the progression of TNBC have not been clarified. We found that down-regulation of ZNF662 in breast cancer was associated with abnormal promoter methylation. ZNF662 over-expression inhibited triple-negative breast cancer cell proliferation, migration and invasion and induced cell cycle arrest in vitro, and also suppressed the growth and metastasis of xenograft tumors in vivo. Further experiments confirmed that ZNF662 could directly bind to the NGF promoter sites and significantly inhibit NGF transcription activity. In addition, ZNF662 could increase the sensitivity of TNBC cells to the EGFR inhibitor lapatinib. Molecular mechanisms revealed that ZNF662 affected downstream PI3K/AKT and STAT3 signaling pathways to inhibit TNBC progression by down-regulating NGF expression. Altogether, we speculated that ZNF662 might become a promising prognostic marker and therapeutic target for early detection and treatment of TNBC.","PeriodicalId":13762,"journal":{"name":"International Journal of Biological Sciences","volume":"21 9","pages":"4081-4097"},"PeriodicalIF":8.2,"publicationDate":"2025-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12223779/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144560074","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0