Immunohistochemistry and western blot were adopted to detect HMGA2 and epithelial-mesenchymal transition (EMT)-related proteins (E-cadherin and N-cadherin) expression in GC tissues and cells, respectively.
The reverse transcription-quantitative polymerase chain reaction was used to determine HIT000218960 and HMGA2 expression levels in GC tissues and cells.
In vitro, overexpression of HMGA2 promoted GC sphere formation and migration in MKN74/MKN28 cells, whereas downregulation of HMGA2 decreased GC sphere formation and migration in MKN45/MGC803 cells.
Increased HMGA2, FOXL2, and ITGA2 levels were associated with reduced overall survival periods of patients with gastric cancer.<b>Conclusions:</b> This study demonstrated that the transactivation of FOXL2 driven by interactions between HMGA2 and pRb might exert critical effects on the metastases and EMT of chemoresistant gastric cancer.
These data demonstrate that miR-33b-5p may be a potential therapeutic target for gastric cancer and function as tumor-suppressive miRNA through targeting HMGA2 in gastric cancer.
Further conclusion showed that coexpression of HMGA2 and Oct4 in gastric cancer correlated with tumor invasion, metastasis, and clinical prognosis and predicted an unfavorable clinical outcome.
Using quantitative real-time reverse transcription-PCR, we analyzed HMGA2 expression with respect to various clinicopathologic factors in 110 patients with gastric cancer.