MOSPD1 facilitates fatty acid metabolism and gastric cancer progression by promoting the MAPK pathway.

Abstract

Background: Motile sperm domain containing 1 (MOSPD1) is overexpressed in colorectal, prostate, and breast cancers, but its role in gastric cancer (GC) progression remains unclear.

Methods: The effect of MOSPD1 was evaluated using cell viability, colony formation, wound healing, and Transwell assays. Triglyceride and lipid levels were measured in GC cells. Western blotting was used to examine protein expression. A mouse model of subcutaneous tumor xenotransplantation was used to evaluate the effects of MOSPD1 knockdown on GC cells.

Results: MOSPD1 expression in GC tissues and cells was higher than in normal tissues and cells. MOSPD1 knockdown decreased the proliferation, migration, and invasion of GC cells and the growth of subcutaneous tumors. MOSPD1 overexpression increased the proliferation, migration, and invasion of GC cells. Levels of triglyceride, lipid, and fatty acid synthesis-related enzymes (ACLY, ACC1, and FASN) were downregulated in MOSPD1 knockdown cells and upregulated in MOSPD1 overexpressed cells. MOSPD1 knockdown inhibited the phosphorylation of ERK, JNK, and P38 in GC cells and subcutaneous tumors. MOSPD1 overexpression promoted the phosphorylation of ERK, JNK, and P38 in GC cells.

Conclusions: High MOSPD1 expression facilitates fatty acid metabolism and GC progression by activating the MAPK pathway. Thus, MOSPD1 may be a potential therapeutic target for GC.