STAT5A reprograms fatty acid metabolism and promotes tumorigenesis of gastric cancer cells.

OBJECTIVE:The aim of this study was to determine the underlying effect of fatty acid metabolism on the tumorigenesis of gastric cancer cells. MATERIALS AND METHODS:The expression patterns of and FASN in gastric cancer were investigated based on the Cancer Genome Atlas (TCGA) database and compared between 40 pairs of cancer samples and adjacent tissues. The pathological significance of duanyu18135A in gastric cancer was explored by GESA assay, and the molecular mechanism of duanyu18135A-mediated FASN expression was investigated by Luciferase assay and ChIP-qPCR. Fatty acid metabolic change was explored by detecting the content of neutral lipid, triglycerides, and phospholipids in duanyu18135A silenced MKN28 and AGS cells. Furthermore, Cell Counting Kit-8 (CCK-8) assay, colony formation, and Mouse xenograft were used to detect the function of duanyu18135A-mediated fatty acid metabolism on tumorigenic ability of gastric cancer cells. RESULTS:Upregulated duanyu18135A in gastric cancer was found to be not only an unconventional risk for over survival of gastric cancer patients, but also associated with fatty acid metabolism signaling. Furthermore, duanyu18135A can regulate the expression of the fatty acid binding protein 5 (FABP5) by binding to the promoter of FABP5 in MKN28 and AGS cells. Functional studies have shown that FABP5 expression promoted the proliferation and tumorigenesis of gastric cancer cells by reprogramming intracellular fatty acid metabolism. CONCLUSIONS:Our results indicate that duanyu18135A-dependent FABP5 expression plays a carcinogenic role in the tumorigenesis of gastric cancer cells via reprogramming intracellular fatty acid metabolism, which establishes a new mechanism for the tumorigenesis of gastric cancer cells.

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