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

• Published in: Gene 2019-10, Vol.716, p.144010-144010, Article 144010
• Main Authors: Yang, Qiong, Deng, Youhui, Xu, Yuanyuan, Ding, Nan, Wang, Chen, Zhao, Xuetong, Lou, Xiaomin, Li, Yongjun, Zhao, Hua, Fang, Xiangdong
• Format: Article
• Language: English
• Subjects: Alternative splicing; Melanoma; SSATX; Tumor suppressor; Wnt signaling pathway
• ISSN: 0378-1119; 1879-0038
• DOI: 10.1016/j.gene.2019.144010

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. •SSATX is a non-coding transcript variant of the SAT1 gene.•Downregulation of SSATX promotes melanoma cell growth, migration, and invasion.•SSATX depletion affects melanoma cell behave independent of SSAT1 expression.•Repression of SSATX activates the Wnt/β-catenin signaling pathway in melanoma cells.