ABSTRACT
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.
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.
ABSTRACT
Baculovirus expression vector system (BEVS) is a powerful and versatile platform for recombinant protein production in insect cells. As the most frequently used baculovirus, Autographa californica multiple nucleopolyhedrovirus (AcMNPV) encodes 155 open reading frames (ORFs), including a considerable number of non-essential genes for the virus replication in cell culture. Studies have shown that protein production in BEVS can be improved by removing some viral dispensable genes, and these AcMNPV vectors also offer the possibility of accommodating larger exogenous gene fragments. In this study, we, respectively, deleted 14 DNA fragments from AcMNPV genome, each of them containing at least two contiguous genes that were known nonessential for viral replication in cell culture or functionally unknown. The effects of these fragment-deletions on virus replication and exogenous protein production were examined. The results showed that 11 of the 14 fragments, containing 43 genes, were dispensable for the virus replication in cultured cells. By detecting the expression of intracellularly expressed and secreted reporter proteins, we demonstrated that nine of the fragment-deletions benefited protein production in Sf9 cells and/or in High Five cells. After combining the deletion of some dispensable fragments, we obtained two AcMNPV vectors shortened by more than 10 kb but displayed an improved capacity for recombinant protein production. The deletion strategies used in this study has the potential to further improve the BEVS.