4.2 Article

Acetyl-CoA Synthetase 2 Promotes Cell Migration and Invasion of Renal Cell Carcinoma by Upregulating Lysosomal-Associated Membrane Protein 1 Expression

期刊

CELLULAR PHYSIOLOGY AND BIOCHEMISTRY
卷 45, 期 3, 页码 984-992

出版社

Cell Physiol Biochem Press GmbH & Co
DOI: 10.1159/000487293

关键词

ACSS2; Renal cell carcinoma; Lipid metabolism; Acetate; Cell migration; Invasion

资金

  1. Natural Science Foundation of Hebei Province [H2014205082]
  2. Shenzhen Key Laboratory fund of Male Reproductive Medicine and Genetics [2014B030301001]
  3. Guangdong Key Laboratory fund of Male Reproductive Medicine and Genetics [2014B030301001]
  4. Shenzhen Foundation of Science and Technology Innovation [JCYJ20160427185401364]

向作者/读者索取更多资源

Background/Aims: Reprogramming energy metabolism is an emerging hallmark of many cancers, and this alteration is especially evident in renal cell carcinomas (RCCs). However, few studies have been conducted on lipid metabolism. This study investigated the function and mechanism of lipid metabolism-related acetyl-CoA synthetase 2 (ACSS2) in RCC development, cell migration and invasion. Methods: Quantitative real-time PCR (qRT-PCR) was used to determine the expression of ACSS2 in cancer tissue and adjacent tissue. The inhibition of ACSS2 expression was achieved by RNA interference, which was confirmed by qRT-PCR and Western blotting. Cell proliferation and apoptosis were detected by a CCK8 assay and a flow cytometry analysis, respectively. Cell migration and invasion were determined by the scratch and transwell assays. Following the knockdown of ACSS2 expression, the expression of the autophagy-related factor LAMP1 was measured by qRT-PCR and Western blotting. Results: Compared to adjacent tissues, ACSS2 expression was upregulated in RCC cancer tissues and positively correlated with metastasis. Inhibition of ACSS2 had no effect on RCC cell proliferation or apoptosis. However, decreased ACSS2 expression was found to inhibit RCC cell migration and invasion. ACSS2 was determined to promote the expression of LAMP1, which can also promote cell migration. This pathway may be considered a potential mechanism through which ACSS2 participates in RCC development. Conclusion: These data suggest that ACSS2 is an important factor for promoting RCC development and is essential for cell migration and invasion, which it promotes by increasing the expression of LAMP1. Taken together, these findings reveal a potential target for the diagnosis and treatment of RCC. (C) 2018 The Author(s) Published by S. Karger AG, Basel

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