DDIT3 and gastric cancer: Our previous studies showed that increased HOXA-AS2 promotes gastric cancer cells proliferation by epigenetically silencing P21/PLK3/DDIT3 expression [15], and HOTAIR function as oncogene through acting as a competing endogenous RNA for miR-331-3P or repressing miR34a by binding to PRC2 to promote the epithelial-to-mesenchymal transition in gastric cancer [13, 19].