KDM1A Acts as an Oncogene and Facilitates the Epithelial Mesenchymal Transition Process in Gastric Cancer

ABSTRACT Background This study is performed to research the biological role of KDM1A in the epithelial mesenchymal transition (EMT) of gastric cancer and investigate the mechanism involved. Methods The KDM1A, Vimentin and E‐cadherin levels were studied, as well as the correlation among them in gastric cancer samples. Gastric cancer cells were transfected with KDM1A overexpression and knockdown, and the cellular infiltration, motility, morphology and F‐actin expression were subsequently identified. For the protein level assessment of EMT, the western blot analysis combined with immunofluorescence was employed. The effect of KDM1A on TGF‐β/Notch signaling was also detected. Results KDM1A was overexpressed in gastric cancer tumor tissues. In the clinical gastric carcinoma samples, the level of KDM1A was linked negatively to the expression of E‐cadherin, while positively to the expression of Vimentin. Among the gastric carcinoma population, the expression of KDM1A was linked to the lymph node metastasis, TNM stage and tumor differentiation. The KDM1A downregulation prohibited the cellular motility, infiltration and F‐actin expression, and suppressed EMT process. KDM1A overexpression exhibited promoting effect on EMT in gastric cancer cells. KDM1A regulated TGF‐β/Notch signaling to affect EMT in gastric cancer cells. Conclusion KDM1A acts as an oncogene and facilitates the epithelial mesenchymal transition process by regulating TGF‐β/Notch signal pathway in gastric cancer cells.