The roles of
lncRNA TSLNC8 and its synergetic effects with
osimertinib remain unknown in
lung cancer. qRT-PCR or western blotting was performed to determine the expression levels of TSLNC8, EGFR and STAT3. Colony formation and MTT assays were used to evaluate cell proliferation. Transwell and wound healing assays were performed to assess migration and invasion abilities. Flow cytometry with
Annexin V/PI staining was used to detect changes in cell apoptosis. Nude mice subcutaneous
tumor model was constructed and used for validating the effects of TSLNC8 and
osimertinib in vivo. Expression of TSLNC8 was down-regulated in clinical
lung cancer tissues and cell lines. TSLNC8 overexpression or
osimertinib administration led to promotion of apoptosis and inhibition of cell proliferation, migration and invasion, as well as deactivation of the EGFR-STAT3 pathway, whereas TSLNC8 knockdown had opposite effects. Moreover, the above effects of
osimertinib were remarkably enhanced by TSLNC8 overexpression and inhibited by TSLNC8 knockdown, respectively. Meanwhile, the effects of TSLNC8 overexpression were reversed by STAT3 activation or EGFR overexpression. In the animal model, combination of TSLNC8 overexpression and
osimertinib administration resulted in efficient suppression of
tumor growth. In this study, we revealed a TSLNC8-EGFR-STAT3 signaling axis in
lung cancer, and TSLNC8 overexpression significantly enhanced the anti-
tumor effects of
osimertinib via inhibiting EGFR-STAT3 signaling.