HMGA1 accelerates the malignant progression of gastric cancer through stimulating EMT.

OBJECTIVE:To clarify the role of HMGA1 in influencing proliferation and migration abilities, and EMT (epithelial-mesenchymal transition) in gastric cancer (GC) cells. MATERIALS AND METHODS:Differential expressions of HMGA1 in GC tissues and normal gastric tissues were analyzed in the GEPIA dataset. Its influence on overall survival of GC patients was evaluated as well. Moreover, HMGA1 levels in GC cells and gastric mucosal cells were detected. Regulatory effects of HMGA1 on the proliferation and migration abilities in SGC7901 and MGC803 cells were assessed through a series of functional experiments. At last, influences of HMGA1 on the expression levels of EMT-related genes, E-cadherin, Snail, and Slug were determined in GC cells. RESULTS:Analysis of data in TCGA GEPIA dataset revealed that HMGA1 was upregulated in GC tissues, and GC patients with a high expression level of HMGA1 suffered poorer prognosis. In addition, HMGA1 was identically upregulated in GC cells, and the overexpression of HMGA1 improved the proliferation and migration abilities of SGC7901 and MGC803 cells, downregulated E-cadherin, and upregulated Snail and Slug in GC cells, while silence of HMAG1 yielded the opposite results CONCLUSIONS: HMGA1 is upregulated in GC tissues and predicts poor prognosis, and it aggravates the progression of GC via stimulating EMT.

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