miR‐548ag functions as an oncogene by suppressing MOB1B in the development of obesity‐related endometrial cancer

Obesity is a high‐risk factor in the development of endometrial cancer (EC). Our previous study observed that miR‐548ag was significantly overexpressed in the sera of obese individuals. Here, we report the function of miR‐548ag and its mechanism in promoting the obesity‐related progression of EC. Th...

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Bibliographic Details
Published in:Cancer science 2023-04, Vol.114 (4), p.1507-1518
Main Authors: Pang, Huai, Wang, Jingzhou, Wei, Qianqian, Liu, Jie, Chu, Xiaolong, Yuan, Chenggang, Yang, Bingqi, Li, Menghuan, Ma, Dingling, Tang, Yihan, Wang, Cuizhe, Zhang, Jun
Format: Article
Language:English
Subjects:
Apoptosis
Bioinformatics
Body fat
Cell culture
Cell growth
Cell Line, Tumor
Cell Movement - genetics
Cell Proliferation - genetics
Deactivation
Endometrial cancer
Endometrial Neoplasms - metabolism
Endometrium
Female
Gene Expression Regulation, Neoplastic
Hippo pathway
Hospitals
Humans
Kinases
Membranes
MicroRNAs
MicroRNAs - genetics
MicroRNAs - metabolism
miR‐548ag
MOB1B
Monoclonal antibodies
Obesity
Obesity - complications
Obesity - genetics
Oncogenes
Oncogenes - genetics
Original
ORIGINAL ARTICLES
Polyclonal antibodies
Reagents
Risk factors
Signal transduction
Tumor cell lines
Womens health
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Summary:Obesity is a high‐risk factor in the development of endometrial cancer (EC). Our previous study observed that miR‐548ag was significantly overexpressed in the sera of obese individuals. Here, we report the function of miR‐548ag and its mechanism in promoting the obesity‐related progression of EC. The content of miR‐548ag was increased in the serum of obese EC individuals. Bioinformatics analysis indicated that the survival rate of EC patients with a higher expression of miR‐548ag was significantly reduced. The Mps One Binder Kinase Activator 1B (MOB1B, the core member of the Hippo signaling pathway) is a direct target gene of miR‐548ag, which is inversely correlated with the expression of miR‐548ag. The overexpression of miR‐548ag enhances the proliferation, invasion, and migration, and inhibits apoptosis by downregulating the expression of MOB1B, leading to the deactivation of the Hippo pathway in EC cell lines and contributing to tumor progression in vivo. Our study has established that miR‐548ag functions as an oncogene by suppressing MOB1B in the development of obesity‐related EC. Our results indicate that miR‐548ag is a promising diagnostic biomarker to understand the role of the MOB1B/YAP1/CCND1/XIAP axis in promoting obesity‐related EC progression. Starting from clinical issues, this study clarified the molecular mechanism of high expression miR‐548ag in the occurrence and development of obesity‐related EC through in vitro and in vivo experiments, which will provide a theoretical basis for the prevention and treatment of EC.
ISSN:1347-9032
1349-7006
DOI:10.1111/cas.15679