LncRNA SSTR5-AS1 promotes esophageal carcinoma through regulating ITGB6/JAK1/STAT3 signaling

Abstract

Abstract Background Esophageal carcinoma (ESCA) is the aggressive cancer which threatens people’s health. LncRNA SSTR5-AS1 is upregulated in ESCA. However, the potential regulatory mechanism of SSTR5-AS1 in ESCA is unknown. Methods GEPIA was used to explore the prognosis of SSTR5-AS1 in ESCA patients. EdU staining was used to detect cell proliferation. Transwell assay was applied for assessing cell invasion and migration. Meanwhile, RNA pull-down and RIP were applied to assess the relationship among SSTR5-AS1, EIF4A3 and ITGB6, and FISH was applied for exploring the localization of SSTR5-AS1 in ESCA cells. Results SSTR5-AS1 was upregulated in ESCA. SSTR5-AS1 downregulation repressed the invasion and migration of ESCA cells, and promoted cells apoptosis. Furthermore, SSTR5-AS1 shRNA upregulated the levels of Bax, cleaved caspase 3 and inhibited p-STAT3, p-JAK1 and Bcl-2 levels. SSTR5-AS1 was distributed in cytoplasm, and it could regulate ITGB6 by interacting with EIF4A3. SSTR5-AS1 silencing inhibited ITGB6 expression and inactivated JAK1/STAT3 signaling, while EIF4A3 upregulation reversed this phenomenon. In addition, SSTR5-AS1 silencing attenuated the malignant behavior of ESCA cells through ITGB6-mediated JAK1/STAT3 signaling. Conclusion SSTR5-AS1 promotes ESCA development through interacting with EIF4A3 to regulate ITGB6/JAK1/STAT3 signaling. Hence, this research supplied a basis for discovering strategies against ESCA.