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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Veröffentlicht in: | Cancer science 2023-04, Vol.114 (4), p.1507-1518 |
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Sprache: | eng |
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Zusammenfassung: | 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. |
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ISSN: | 1347-9032 1349-7006 |
DOI: | 10.1111/cas.15679 |