科研成果详情

题名Glucose dysregulation promotes oncogenesis in human bladder cancer by regulating autophagy and YAP1/TAZ expression
作者
发表日期2023-09-04
发表期刊Journal of cellular and molecular medicine   影响因子和分区
语种英语
原始文献类型Journal Article
关键词AMPK YAP1/TAZ autophagy bladder cancer high glucose
其他关键词HIPPO ; TRANSPLANTATION
摘要Glucose dysregulation is strongly correlated with cancer development, and cancer is prevalent in patients with Type 2 diabetes (T2D). We aimed to elucidate the mechanism underlying autophagy in response to glucose dysregulation in human bladder cancer (BC). 220 BC patients were included in this retrospective study. The expression of YAP1, TAZ and AMPK, EMT-associated markers, and autophagy marker proteins was analysed by immunohistochemistry, western blotting, and quantitative real-time PCR (qPCR). Further, T24 and UMUC-3 BC cells were cultured in media with different glucose concentrations, and the expression of YAP1, TAZ, AMPK and EMT-associated markers, and autophagy marker proteins was analysed by western blotting and qPCR. Autophagy was observed by immunofluorescence and electron microscopy. BC cell viability was tested using MTT assays. A xenograft nude mouse model of diabetes was used to evaluate tumour growth, metastasis and survival. A poorer pathologic grade and tumour-node-metastasis stage were observed in patients with BC with comorbid T2D than in others with BC. YAP1 and TAZ were upregulated in BC samples from patients with T2D. Mechanistically, high glucose (HG) promoted BC progression both in vitro and in vivo and inhibited autophagy. Specifically, various autophagy marker proteins and AMPK were negatively regulated under HG conditions and correlated with YAP1 and TAZ expression. These results demonstrate that HG inhibits autophagy and promotes cancer development in BC. YAP1/TAZ/AMPK signalling plays a crucial role in regulating glucose dysregulation during autophagy. Targeting these effectors exhibits therapeutic significance and can serve as prognostic markers in BC patients with T2D.
资助项目China Scholarship Council[202108330204];Key Laboratory of Clinical Laboratory Diagnosis and Translational Research of Zhejiang Province[2022E10022];National Natural Science Foundation of China[81902555];Wenzhou Municipal Science and Technology Bureau[Y2020150];Youth Science and Technology Talent Innovation Project of Hainan Provincial Association for Science and Technology[QCXM202017]
出版者WILEY
ISSN1582-1838
EISSN1582-4934
卷号27期号:23页码:3744-3759
DOI10.1111/jcmm.17943
页数16
WOS类目Cell Biology ; Medicine, Research & Experimental
WOS研究方向Cell Biology ; Research & Experimental Medicine
WOS记录号WOS:001061592200001
收录类别PUBMED ; SCIE ; SCOPUS
在线发表日期2023-09
URL查看原文
PubMed ID37665055
SCOPUSEID2-s2.0-85169701176
通讯作者地址[Li, Shi]Department of Urology,Key Laboratory of Clinical Laboratory Diagnosis and Translational Research of Zhejiang Province,The First Affiliated Hospital of Wenzhou Medical University,Zhejiang,Wenzhou,China ; [Yu, Zhixian]Department of Urology,The First Affiliated Hospital of Wenzhou Medical University,Zhejiang,Wenzhou,China ; [Zhu, Hua]Department of Obstetrics and Gynecology,The First Affiliated Hospital of Wenzhou Medical University,Zhejiang,Wenzhou,China
Scopus学科分类Molecular Medicine;Cell Biology
TOP期刊TOP期刊
引用统计
文献类型期刊论文
条目标识符https://kms.wmu.edu.cn/handle/3ETUA0LF/182750
专题附属第一医院
第一临床医学院(信息与工程学院)、附属第一医院_内科学_神经内科
通讯作者Li, Shi; Zhu, Hua; Yu, Zhixian
作者单位
1.Department of Urology,Key Laboratory of Clinical Laboratory Diagnosis and Translational Research of Zhejiang Province,The First Affiliated Hospital of Wenzhou Medical University,Zhejiang,Wenzhou,China;
2.Department of Oncology of The First Affiliated Hospital and Tumor Institute,Hainan Medical University,Hainan,Haikou,China;
3.Department of Urology and Chest Surgery,The People Hospital of Tongjiang,Sichuan,Bazhong,China;
4.Department of Oncology and Hematology,The People Hospital of Tongjiang,Sichuan,Bazhong,China;
5.Cancer Center,Sichuan Academy of Medical Sciences and Sichuan Provincial People's Hospital,Hospital of the University of Electronic Science and Technology of China,Chengdu,China;
6.Department of Urology,The First Affiliated Hospital of Wenzhou Medical University,Wenzhou,China;
7.Department of Neurology,The First Affiliated Hospital of Wenzhou Medical University,Wenzhou,China;
8.Department of Obstetrics and Gynecology,The First Affiliated Hospital of Wenzhou Medical University,Wenzhou,China
第一作者单位附属第一医院
通讯作者单位附属第一医院
第一作者的第一单位附属第一医院
推荐引用方式
GB/T 7714
Li, Shi,Ruan, Banzhan,Wang, Zhi,et al. Glucose dysregulation promotes oncogenesis in human bladder cancer by regulating autophagy and YAP1/TAZ expression[J]. Journal of cellular and molecular medicine,2023,27(23):3744-3759.
APA Li, Shi., Ruan, Banzhan., Wang, Zhi., Xia, Jianling., Lin, Qi., ... & Yu, Zhixian. (2023). Glucose dysregulation promotes oncogenesis in human bladder cancer by regulating autophagy and YAP1/TAZ expression. Journal of cellular and molecular medicine, 27(23), 3744-3759.
MLA Li, Shi,et al."Glucose dysregulation promotes oncogenesis in human bladder cancer by regulating autophagy and YAP1/TAZ expression".Journal of cellular and molecular medicine 27.23(2023):3744-3759.

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