LncRNA MIR200CHG inhibits EMT in gastric cancer by stabilizing miR-200c from target-directed miRNA degradation

Yixiao Zhu, Chengmei Huang, Chao Zhang, Yi Zhou, Enen Zhao, Yaxin Zhang, Xingyan Pan, Huilin Huang (), Wenting Liao () and Xin Wang ()
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Yixiao Zhu: Sun Yat-sen University Cancer Center
Chengmei Huang: Sun Yat-sen University Cancer Center
Chao Zhang: Sun Yat-sen University Cancer Center
Yi Zhou: Sun Yat-sen University Cancer Center
Enen Zhao: Sun Yat-sen University Cancer Center
Yaxin Zhang: Sun Yat-sen University Cancer Center
Xingyan Pan: Sun Yat-sen University Cancer Center
Huilin Huang: Sun Yat-sen University Cancer Center
Wenting Liao: Sun Yat-sen University Cancer Center
Xin Wang: The Chinese University of Hong Kong

Nature Communications, 2023, vol. 14, issue 1, 1-19

Abstract: Abstract Gastric cancer (GC) is a heterogeneous disease, threatening millions of lives worldwide, yet the functional roles of long non-coding RNAs (lncRNAs) in different GC subtypes remain poorly characterized. Microsatellite stable (MSS)/epithelial-mesenchymal transition (EMT) GC is the most aggressive subtype associated with a poor prognosis. Here, we apply integrated network analysis to uncover lncRNA heterogeneity between GC subtypes, and identify MIR200CHG as a master regulator mediating EMT specifically in MSS/EMT GC. The expression of MIR200CHG is silenced in MSS/EMT GC by promoter hypermethylation, associated with poor prognosis. MIR200CHG reverses the mesenchymal identity of GC cells in vitro and inhibits metastasis in vivo. Mechanistically, MIR200CHG not only facilitates the biogenesis of its intronic miRNAs miR-200c and miR-141, but also protects miR-200c from target-directed miRNA degradation (TDMD) through direct binding to miR-200c. Our studies reveal a landscape of a subtype-specific lncRNA regulatory network, providing clinically relevant biological insights towards MSS/EMT GC.

Date: 2023
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DOI: 10.1038/s41467-023-43974-w

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