It also promoted the proliferation, cloning, and invasion of esophageal cancer cells.6, 102 SNHG1 could activate the NOTCH and EMT pathway to augment cancer cell invasion and growth, while SNHG1 sponged MIR338 to increase the expression of CST3 and to downregulate CASP8/3.6, 102 Regarding GAS5, in contrast to other digestive cancers types, Li W et al showed that GAS5 no longer acted as a tumor suppressor gene but acted as an oncogene in esophageal cancer. This evidence concerns the gene CST3 and esophageal cancer.