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Tumor‐suppressive functions of long‐chain acyl‐CoA synthetase 4 in gastric cancer
Author(s) -
Ye Xiaojuan,
Zhang Yi,
Wang Xiao,
Li Yandong,
Gao Yong
Publication year - 2016
Publication title -
iubmb life
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.132
H-Index - 113
eISSN - 1521-6551
pISSN - 1521-6543
DOI - 10.1002/iub.1486
Subject(s) - gene knockdown , immunohistochemistry , cell growth , cancer research , biology , carcinogenesis , cell , ectopic expression , western blot , cancer , microbiology and biotechnology , arachidonic acid , chemistry , enzyme , biochemistry , immunology , gene , genetics
Long chain acyl CoA synthetase 4 (ACSL4) is a key enzyme in fatty acid metabolism with marked preference for arachidonic acid (AA). Recent reports have implicated its crucial roles in tumorigenesis. However in gastric cancer (GC), the expression and function of ACSL4 remain unclear. In the present study, we identified ACSL4 as a potential tumor suppressor in GC. The ACSL4 expression in GC samples was evaluated by real‐time PCR and immunohistochemistry. The results indicated that the mRNA and protein levels of ACSL4 were frequently downregulated in cancer tissues compared with the adjacent non‐cancerous mucosa control tissues. Cell‐based functional assays exhibited that ectopic expression of ACSL4 inhibits cell growth, colony formation and cell migration, whereas ACSL4 knockdown enhanced these effects. In a nude mice model, ACSL4 knockdown also promoted subcutaneous xenografts' growth in vivo . Moreover, western blot analysis revealed that ACSL4 expression had a significant effect on FAK and P21 protein level. These findings suggest that ACSL4 plays a tumor‐suppressive role and could be a potential therapeutic target in GC. © 2016 IUBMB Life, 68(4):320–327, 2016