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Abstract 477: Down-regulated miR-23a contributes to invasion and metastasis of cutaneous melanoma by promoting autophagy

Authors :
Tianwen Gao
Weinan Guo
Weigang Zhang
Lin Liu
Chunying Li
Huina Wang
Yuqi Yang
Qiong Shi
Ling Liu
Sen Guo
Gang Wang
Zhe Jian
Tao Zhao
Source :
Cancer Research. 77:477-477
Publication Year :
2017
Publisher :
American Association for Cancer Research (AACR), 2017.

Abstract

Background: The occurrence of invasion and metastasis is the major cause of mortality in melanoma. Recent studies suggest that dysregulated miRNAs play critical roles in this procedure, but the underlying mechanism remains elusive. Here, we show that down-regulated miR-23a can promote invasion-metastasis cascade through autophagy in melanoma.Methods: The role of miR-23a in prognosis was assessed in a cohort of melanoma patients (n = 192) with Kaplan-Meier analysis. The effects of miR-23a overexpression were investigated using assays of invasion, migration and in a xenograft model (n = 10 mice per group). Autophagy-related target of miR-23a was confirmed by bioinformatics analysis, luciferase assays and immunoblotting. Molecular studies were performed to determine the downstream cellular and molecular mechanisms. All statistical tests were two-sided.Results: Serum miR-23a level was significantly down-regulated in melanoma patients (P< .001) and was highly correlated with poor clinical outcomes (P = .027, log-rank test). In addition, miR-23a level was remarkably decreased in metastatic melanoma tissues and cell lines (P Note: This abstract was not presented at the meeting. Citation Format: Weinan Guo, Huina Wang, Yuqi Yang, Sen Guo, Weigang Zhang, Tao Zhao, Lin Liu, Zhe Jian, Ling Liu, Gang Wang, Tianwen Gao, Qiong Shi, Chunying Li. Down-regulated miR-23a contributes to invasion and metastasis of cutaneous melanoma by promoting autophagy [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 477. doi:10.1158/1538-7445.AM2017-477

Details

ISSN :
15387445 and 00085472
Volume :
77
Database :
OpenAIRE
Journal :
Cancer Research
Accession number :
edsair.doi...........e1ef1cededfe503c42641753d80938d0