Research Papers:

Deregulation of miR-183 promotes melanoma development via lncRNA MALAT1 regulation and ITGB1 signal activation

Yong Sun, Hongyu Cheng, Guangjun Wang, Guojun Yu, Dawei Zhang, Yibing Wang, Wei Fan and Weixi Yang _

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Oncotarget. 2017; 8:3509-3518. https://doi.org/10.18632/oncotarget.13862

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Yong Sun1,*, Hongyu Cheng1,*, Guangjun Wang1, Guojun Yu1, Dawei Zhang1, Yibing Wang1, Wei Fan2, Weixi Yang1

1Department of Burn and Plastic Surgery, Huai’an First People’s Hospital, Nanjing Medical University, Huai’an, China

2Department of Anesthesiology, Huai’an First People’s Hospital, Nanjing Medical University, Huai’an, China

*These authors have contributed equally to this work

Correspondence to:

Wei Fan, email: [email protected]

Weixi Yang, email: [email protected]

Keywords: miR-183, MALAT1, ITGB1, melanoma, competitive endogenous RNA

Received: September 01, 2016    Accepted: November 22, 2016    Published: December 10, 2016


Dysregulation of miR-183 has been recently elucidated in several carcinomas. However, the expression patterns and mechanisms of miR-183 involved in malignant melanoma remain unidentified. Here, we found down-regulation of miR-183 in melanoma tissues and cells. Decreased level of miR-183 was relevant to poor overall survival, while miR-183 up-regulation resulted in a marked suppression of cell growth in vitro and in vivo. We further found that the expression and function of miR-183 were suppressed by MALAT1. Integrin β1 (ITGB1) was then speculated and confirmed as a direct target of miR-183. We also illustrated that MALAT1 may function as a sponge competitive endogenous RNA (ceRNA) for miR-183, and thus regulate the molecular expression of ITGB1. Collectively, we found a new signaling pathway promoting melanoma development by MALAT1-miR-183-ITGB1 axis, which may be clinically valuable as new targets for malignant melanoma therapy.

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