Acyl-CoA synthetase long-chain 3 regulates AKT phosphorylation and the functional activity of human prostate cancer cells

Ke Li, Y. Mao, Wenhan Qiu, Jianwen He, Dejuan Wang, Cheng Hu, Wen-tao Huang, S. Jie, J. Qiu
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引用次数: 1

Abstract

Abstract Metastasis is the main cause of cancer-specific death in patients with prostate cancer (PCa). Acyl-coenzyme A synthetase long-chain family member 3 (ACSL3) is involved in the metabolic reprogramming of multiple types of cancer cells, but its role in PCa metastasis remains largely unknown. Here, we determined the effect of overexpression or small interfering RNA-mediated depletion of ACSL3 on the migratory and invasive abilities of human PCa cell lines. We also conducted phospho-protein microarray analysis to identify signaling pathway components affected by ACSL3 modulation. Overexpression of ACSL3 promoted the migration and invasion of PCa cells, whereas ACSL3 downregulation had the opposite effects. Mechanistically, phospho-protein analysis showed that ACSL3 regulated the phosphorylation of AKT and the expression of matrix metalloproteinase9. Our results support a potential role for ACSL3 in promoting the metastatic behavior of PCa, possibly via AKT/matrix metalloproteinase9 pathways. Thus, ACSL3 could be a novel target for the development of treatments for PCa.
酰基辅酶a合成酶长链3调控AKT磷酸化和人前列腺癌细胞的功能活性
转移是前列腺癌(PCa)患者癌症特异性死亡的主要原因。酰基辅酶A合成酶长链家族成员3 (ACSL3)参与多种类型癌细胞的代谢重编程,但其在前列腺癌转移中的作用尚不清楚。在这里,我们确定了过表达或小干扰rna介导的ACSL3缺失对人PCa细胞系迁移和侵袭能力的影响。我们还进行了磷酸化蛋白微阵列分析,以确定受ACSL3调节影响的信号通路成分。ACSL3的过表达促进了PCa细胞的迁移和侵袭,而ACSL3的下调则起到相反的作用。磷酸化蛋白分析表明,ACSL3调控AKT磷酸化和基质金属蛋白酶9的表达。我们的研究结果支持ACSL3在促进前列腺癌转移行为中的潜在作用,可能通过AKT/基质金属蛋白酶9途径。因此,ACSL3可能成为PCa治疗发展的新靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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