Knockdown of SSATX, an alternative splicing variant of the SAT1 gene, promotes melanoma progression

SAT1 基因的可变剪接变体 SSATX 的敲除会促进黑色素瘤的进展

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作者:Qiong Yang, Youhui Deng, Yuanyuan Xu, Nan Ding, Chen Wang, Xuetong Zhao, Xiaomin Lou, Yongjun Li, Hua Zhao, Xiangdong Fang

Abstract

Alternative splicing can generate multiple protein messages from a single gene and has emerged as an important mechanism to regulate cancer pathways. The human SAT1 gene produces two transcript variants: one translates spermidine/spermine N-1 acetyltransferase (SSAT1), the rate-limiting enzyme in the catabolism of polyamines, and the other generates SSATX, which has largely unknown biological functions. Here, we used experimental data and analyses of several melanoma transcriptome datasets to reveal that SSATX is weakly expressed in melanoma cells. SSATX knockdown promoted the proliferation, migration, and invasion of human melanoma cells via the activation of the Wnt signaling pathway in a manner that was independent of SSAT1 expression. Based on our data, we propose that SSATX functions as a long non-coding RNA prior to its degradation in melanoma cells. Overall, our findings indicate that SSATX acts as a tumor suppressor, which may aid the future diagnosis and treatment of melanoma.

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