Cancer gene therapy最新文献

Retraction Note: Circular RNA hsa_circ_0009172 suppresses gastric cancer by regulation of microRNA-485-3p-mediated NTRK3.

IF 4.8 3区医学

Cancer gene therapy Pub Date : 2024-12-18 DOI: 10.1038/s41417-024-00870-9

Hao Wang, Nan Wang, Xiaoli Zheng, Lei Wu, Chengcheng Fan, Xue Li, Ke Ye, Suxia Han

引用次数: 0

ITGA3 promotes pancreatic cancer progression through HIF1α- and c-Myc-driven glycolysis in a collagen I-dependent autocrine manner.

IF 4.8 3区医学

Cancer gene therapy Pub Date : 2024-12-17 DOI: 10.1038/s41417-024-00864-7

Rongkun Li, Qian Ji, Shengqiao Fu, Jichun Gu, Dejun Liu, Lu Wang, Xiao Yuan, Yi Wen, Chunhua Dai, Hengchao Li

{"title":"ITGA3 promotes pancreatic cancer progression through HIF1α- and c-Myc-driven glycolysis in a collagen I-dependent autocrine manner.","authors":"Rongkun Li, Qian Ji, Shengqiao Fu, Jichun Gu, Dejun Liu, Lu Wang, Xiao Yuan, Yi Wen, Chunhua Dai, Hengchao Li","doi":"10.1038/s41417-024-00864-7","DOIUrl":"10.1038/s41417-024-00864-7","url":null,"abstract":"Pancreatic cancer is characterized by severe metabolic stress due to its prominent desmoplasia and poor vascularization. Integrin subunit alpha 3 (ITGA3) is a cell surface adhesion protein involved in tumor progression. However, the role of ITGA3 in pancreatic cancer progression, especially in metabolic reprogramming, remains largely unknown. In this study, we found that ITGA3 expression is elevated in pancreatic cancer tissues and predicts poor prognosis for patients with pancreatic cancer. Functional assays revealed that ITGA3 promotes the growth and liver metastasis of pancreatic cancer via boosting glycolysis. Mechanistically, Collagen I (Col1) derived from cancer cells acts as a ligand for ITGA3 to activate the FAK/PI3K/AKT/mTOR signaling pathway in an autocrine manner, thereby increasing the expression of HIF1α and c-Myc, two critical regulators of glycolysis. Blockade of Col1 by siRNA or of ITGA3 by a blocking antibody leads to specific inactivation of the FAK/PI3K/AKT/mTOR pathway and impairs malignant tumor behaviors induced by ITGA3. Thus, our data indicate that ITGA3 enhances glycolysis to promote pancreatic cancer growth and metastasis via increasing HIF1α and c-Myc expression in a Col1-dependent autocrine manner, making ITGA3 as a candidate diagnostic biomarker and a potential therapeutic target for pancreatic cancer.","PeriodicalId":9577,"journal":{"name":"Cancer gene therapy","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2024-12-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142846155","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

LRP11-AS1 mediates enterotoxigenic Bacteroides fragilis-related carcinogenesis in colorectal Cancer via the miR-149-3p/CDK4 pathway. LRP11-AS1通过miR-149-3p/CDK4途径介导肠毒性脆弱拟杆菌相关的结直肠癌致癌作用

IF 4.8 3区医学

Cancer gene therapy Pub Date : 2024-12-13 DOI: 10.1038/s41417-024-00862-9

Zhongguang Wu, Mengqiu Yu, Yu Zeng, Yingfeng Huang, Weidong Zheng

引用次数: 0

The deubiquitinating enzyme ATXN3 promotes hepatocellular carcinoma progression by stabilizing TAZ.

IF 4.8 3区医学

Cancer gene therapy Pub Date : 2024-12-13 DOI: 10.1038/s41417-024-00869-2

Yuanhao Peng, Hui Nie, Kuo Kang, Xuanxuan Li, Yongguang Tao, Yangying Zhou

{"title":"The deubiquitinating enzyme ATXN3 promotes hepatocellular carcinoma progression by stabilizing TAZ.","authors":"Yuanhao Peng, Hui Nie, Kuo Kang, Xuanxuan Li, Yongguang Tao, Yangying Zhou","doi":"10.1038/s41417-024-00869-2","DOIUrl":"https://doi.org/10.1038/s41417-024-00869-2","url":null,"abstract":"Hepatocellular carcinoma (HCC) was a primary cause of cancer-related morbidity and mortality in China. ATXN3 was a deubiquitinase (DUB) associated with spinocerebellar ataxia, widely expressed in the cytoplasm and nucleus of cells in the central nervous system and other tissues. The crucial role of the Hippo pathway in tumorigenesis has been established, among which TAZ served as one of the key molecules. However, the mechanisms underlying the deubiquitinase and TAZ in HCC remained largely unknown. In the present study, we explored that ATXN3 was overexpressed in HCC. ATXN3 promoted the proliferation, migration, invasion, and tumorigenic ability of HCC in vitro and in vivo. Besides, we explored that ATXN3 was positively associated with TAZ in HCC. ATXN3 could interact with, stabilize, and deubiquitylate TAZ in a deubiquitylase-dependent manner. Specifically, this interaction was primarily mediated by the C-terminal domain of TAZ and Josephin domain of ATXN3, thereby inhibiting the K48-linked ubiquitin chain on TAZ. Furthermore, we demonstrated that ATXN3 promoted the occurrence and development of HCC by regulating TAZ. Therefore, our study revealed the oncogenic function of ATXN3 and an interesting deubiquitination mechanism of ATXN3 and TAZ in HCC, providing new insights into the diagnosis and treatment of HCC.","PeriodicalId":9577,"journal":{"name":"Cancer gene therapy","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2024-12-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142821955","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

N⁶-methyladenosine modification of RIMS binding protein 2 promotes head and neck squamous cell carcinoma proliferation and radiotherapy tolerance through endoplasmic reticulum stress.

IF 4.8 3区医学

Cancer gene therapy Pub Date : 2024-12-09 DOI: 10.1038/s41417-024-00863-8

Xinyu Sun, Yanshu Zhang, Huirong Wang, Xi Pu, Xiao Yuan, Yuntong Liang, Hao Liu, Xu Wang, Hanqiang Lu

{"title":"N6-methyladenosine modification of RIMS binding protein 2 promotes head and neck squamous cell carcinoma proliferation and radiotherapy tolerance through endoplasmic reticulum stress.","authors":"Xinyu Sun, Yanshu Zhang, Huirong Wang, Xi Pu, Xiao Yuan, Yuntong Liang, Hao Liu, Xu Wang, Hanqiang Lu","doi":"10.1038/s41417-024-00863-8","DOIUrl":"https://doi.org/10.1038/s41417-024-00863-8","url":null,"abstract":"Insulin-like growth factor binding protein 2 (IGF2BP2) fulfills a key role in the development of head and neck squamous cell carcinoma (HNSCC). Radiotherapy is an effective method to treat HNSCC; however, radiation resistance is the main reason for treatment failure. At present, the carcinogenic role of IGF2BP2 in terms of the proliferation of HNSCC and the radioresistance of its therapy remain poorly understood. In the present study, patients with HNSCC with higher IGF2BP2 expression levels were associated with shorter survival times. IGF2BP2 is significantly upregulated in HNSCC cells compared with irradiated cell. Based on functional studies, IGF2BP2 was found to promote HNSCC cell proliferation and tolerance to radiotherapy both in vitro and in vivo. In terms of the underlying mechanism, RIMS binding protein 2 (RIMBP2) was found to be highly expressed in HNSCC and to promote the proliferation of HNSCC and radiotherapy resistance. RIMBP2 was shown to be a direct target of IGF2BP2, activating endoplasmic reticulum stress in HNSCC. In addition, it has been demonstrated that IGF2BP2, as m6A reader, is able to promote RIMBP2 stability via binding to m6A sites in the RIMBP2-coding sequence region. Therefore, the present study has unveiled a potential mechanism via which IGF2BP2 promotes HNSCC development and radiotherapy resistance; moreover, from a therapeutic perspective, IGF2BP2 may serve as a potential therapeutic target and a valuable prognostic biomarker for patients with HNSCC who have developed tolerance towards radiotherapy.","PeriodicalId":9577,"journal":{"name":"Cancer gene therapy","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2024-12-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142799455","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

Editorial Expression of Concern: E1A-induced apoptosis does not prevent replication of adenoviruses with deletion of E1b in majority of infected cancer cells.

IF 4.8 3区医学

Cancer gene therapy Pub Date : 2024-12-04 DOI: 10.1038/s41417-024-00860-x

Xiao-Mei Rao, Michael T Tseng, Xinyu Zheng, Yanbin Dong, Azemat Jamshidi-Parsian, Timothy C Thompson, Malcolm K Brenner, Kelly M McMasters, Heshan Sam Zhou

引用次数: 0

Correction: A model of breast cancer meningeal metastases: characterization with in vivo molecular imaging 更正：乳腺癌脑膜转移模型：活体分子成像特征。

IF 4.8 3区医学

Cancer gene therapy Pub Date : 2024-11-26 DOI: 10.1038/s41417-024-00800-9

Darshini Kuruppu, Deepak Bhere, Christian T. Farrar, Khalid Shah, Anna-Liisa Brownell, Kenneth K. Tanabe

引用次数: 0

CCDC34 maintains stemness phenotype through β-catenin-mediated autophagy and promotes EGFR-TKI resistance in lung adenocarcinoma. CCDC34通过β-catenin介导的自噬维持干性表型，并促进肺腺癌对表皮生长因子受体-TKI的耐药性。

IF 4.8 3区医学

Cancer gene therapy Pub Date : 2024-11-25 DOI: 10.1038/s41417-024-00843-y

Ping Yue, Yuchao He, Ran Zuo, Wenchen Gong, Yu Wang, Liwei Chen, Yi Luo, Yuanying Feng, Yuan Gao, Zhiyong Liu, Peng Chen, Hua Guo

{"title":"CCDC34 maintains stemness phenotype through β-catenin-mediated autophagy and promotes EGFR-TKI resistance in lung adenocarcinoma.","authors":"Ping Yue, Yuchao He, Ran Zuo, Wenchen Gong, Yu Wang, Liwei Chen, Yi Luo, Yuanying Feng, Yuan Gao, Zhiyong Liu, Peng Chen, Hua Guo","doi":"10.1038/s41417-024-00843-y","DOIUrl":"https://doi.org/10.1038/s41417-024-00843-y","url":null,"abstract":"Despite recent advances in treatment strategy, lung cancer remains the leading cause of cancer-related mortality worldwide, and it is a serious threat to human health. Lung adenocarcinoma (LUAD) is the most common histological type of lung cancer, and approximately 40-50% of patients with LUAD in Asian populations have epidermal growth factor receptor (EGFR) mutations. The use of EGFR tyrosine kinase inhibitors (EGFR-TKIs) has revolutionarily improved the prognosis of patients with EGFR-mutated LUAD. However, acquired drug resistance is the main cause of treatment failure. Therefore, new therapeutic strategies are necessary to address the resistance to EGFR-TKIs in patients with LUAD. Cancer stemness-related factors lead to multiple-drug resistance in cancer treatment, including EGFR-TKI resistance. Coiled-coil domain-containing 34 (CCDC34) serves as an oncogene in several types of cancer. However, the role and molecular mechanism of CCDC34 in the malignant progression of LUAD have not been reported to date. In the present study, we found that CCDC34 may be associated with LUAD stemness through weighted gene co-expression network analysis (WGCNA). Furthermore, we demonstrated that CCDC34 promoted LUAD stemness properties through β-catenin-mediated regulation of ATG5-induced autophagy, which was conducive to acquired EGFR-TKI resistance in LUAD in vitro and in vivo. Knockdown CCDC34 can synergistically inhibit tumor growth when combined with EGFR-TKIs. This study reveals a positive association between CCDC34 and the stemness phenotype of LUAD, providing new insights into overcoming EGFR-TKI resistance in LUAD by inhibiting CCDC34 expression.","PeriodicalId":9577,"journal":{"name":"Cancer gene therapy","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2024-11-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142715498","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

Soft tissue sarcomas at the single-cell and spatial resolution: new markers and targets. 单细胞和空间分辨率的软组织肉瘤：新的标记和靶标。

IF 4.8 3区医学

Cancer gene therapy Pub Date : 2024-11-24 DOI: 10.1038/s41417-024-00856-7

Maxim E Menyailo, Elena E Kopantseva, Anna A Khozyainova, Anastasia A Korobeynikova, Evgeny V Denisov

引用次数: 0

Establishment and characterization of the first immortalized vocal cord leukoplakia epithelial cell line. 建立首个永生化声带白斑上皮细胞系并确定其特征。

IF 4.8 3区医学

Cancer gene therapy Pub Date : 2024-11-23 DOI: 10.1038/s41417-024-00859-4

Zi-Ming Fu, Yang-Yang Bao, Zhe Chen, Jiang-Tao Zhong, Heng-Chao Chen, Zai-Zai Cao, Shui-Hong Zhou

引用次数: 0