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

Aim: To investigate function of somatostatin receptor 5 antisense RNA 1 (SSTR5-AS1) in esophageal carcinoma (ESCA). Materials & methods: The cellular function was assessed using EdU staining and Transwell assay. The localization of SSTR5-AS1 was measured using fluorescence in situ hybridization staining. Results: SSTR5-AS1 shRNA repressed invasion and migration and induced apoptosis in ESCA cells. SSTR5-AS1 was distributed in cytoplasm, and it regulated its subunit integrin beta 6 (ITGB6) via eukaryotic translation initiation factor 4A3 (EIF4A3). SSTR5-AS1 shRNA inactivated ITGB6 and JAK1/STAT3 signaling. SSTR5-AS1 silencing attenuated the malignant behavior of ESCA cells through the ITGB6-mediated JAK1/STAT3 axis. Conclusion: SSTR5-AS1 promotes tumorigenesis of ESCA by interacting with EIF4A3 to regulate ITGB6/JAK1/STAT3 axis, which serves a basis for discovering strategies against ESCA. PLAIN LANGUAGE SUMMARY The development of esophageal carcinoma (ESCA) seriously affects the health of people. Although great efforts have been made for curing ESCA, the outcomes remain limited. In this research, we used large amounts of experiments about the molecular biology. As expected, we found knockdown of lncRNA SSTR5-AS1 could inhibit the tumorigenesis of ESCA through mediation of its subunit integrin beta 6 /JAK1/STAT3 axis. Thus, our research provided new molecular targets for ESCA treatment.