HMGA 2 is associated with the aggressiveness of tongue squamous cell carcinoma

Objective To analyze the effects of HMGA 2 on proliferation, invasion, and metastasis in tongue squamous cell carcinoma ( TSCC ). Methods HMGA 2 knockdown was performed in SCC 15 cell lines, and functional assay was applied to observe the effects on cell migration and invasion. Real‐time PCR , Western blotting, and immunohistochemistry ( IHC ) were also used to measure the expression of HMGA 2 and EMT markers. Results HMGA 2 expression was decreased after lentivirus infection. Functional assay showed that silence of HMGA 2 can inhibit the proliferation of SCC 15 cells and arrest the cells in G1/S phase. Moreover, knockdown of HMGA 2 enhanced apoptosis of SCC 15 cells. Wound‐healing assay and transwell assay indicated that knockdown of HMGA 2 significantly inhibited migration and invasion ability of SCC 15 cells. Expression detection suggested that HMGA 2 may be involved in the metastasis of SCC 15 cells by activating Twist family expression and inducing epithelial–mesenchymal transition ( EMT ) process. IHC analysis showed that HMGA 2 and vimentin were up‐regulated in TSCC tissues, while E‐cadherin was down‐regulated. Clinicopathological analysis indicated that expression of HMGA 2, E‐cadherin, and Vimentin were associated with recurrence of patients with TSCC . Conclusion Our findings demonstrated that HMGA 2 may promote malignant transformation of TSCC through EMT process and may be an independent prognosis biomarker for TSCC .