Xu-Dong Xiang1, Jing Yu2, Gao-Feng Li3, Lin Xie4, Heng Li5. 1. Department of Thoracic Surgery, Third Affiliated Hospital of Kunming Medical University, Kunming 650118, China. 2. Department of Gynecologic Oncology, Third Affiliated Hospital of Kunming Medical University, Kunming 650118, China. 3. Department of Thoracic Surgery, Third Affiliated Hospital of Kunming Medical University, Kunming 650118, China. Electronic address: 15969591603@139.com. 4. Department of Medical Oncology, Third Affiliated Hospital of Kunming Medical University, Kunming 650118, China. 5. Kunming Medical University, Kunming 650118, China.
Abstract
OBJECTIVE: To investigate the effect and mechanism of inhibitor everolimus on EGFR-TKI resistance NSCLC. METHODS: MTT assay was used to detect proliferation of human non-small cell lung cancer cell line A549. Flow cytometry was used to detect the changes of apoptosis and cycle distribution in each group after 24 h and 48 h. RT-PCR was used to detect the changes of PTEN and 4EBP1 expression levels after 48 h of monotherapy and combination therapy. RESULTS: MTT assay showed that everolimus had dose-dependent inhibition against growth of A549 cells. Flow cytometry showed when everolimus could induce apoptosis and induce G0/G1 phase cell cycle arrest, which was time-dependent (P<0.05). RT-PCR showed everolimus could increase PTEN and 4EBP1 expression. CONCLUSIONS: mTOR inhibitor everolimus has an inhibitory effect on EGFR-TKI resistant NSCLC, which cannot reverse the resistance effect of EGFR-TKI resistant cell line A549. The relationship between EGFR/AKT signaling pathway and the mTOR signaling pathway and the mechanism in non-small cell lung cancer need further study.
OBJECTIVE: To investigate the effect and mechanism of inhibitor everolimus on EGFR-TKI resistance NSCLC. METHODS:MTT assay was used to detect proliferation of humannon-small cell lung cancer cell line A549. Flow cytometry was used to detect the changes of apoptosis and cycle distribution in each group after 24 h and 48 h. RT-PCR was used to detect the changes of PTEN and 4EBP1 expression levels after 48 h of monotherapy and combination therapy. RESULTS:MTT assay showed that everolimus had dose-dependent inhibition against growth of A549 cells. Flow cytometry showed when everolimus could induce apoptosis and induce G0/G1 phase cell cycle arrest, which was time-dependent (P<0.05). RT-PCR showed everolimus could increase PTEN and 4EBP1 expression. CONCLUSIONS:mTOR inhibitor everolimus has an inhibitory effect on EGFR-TKI resistant NSCLC, which cannot reverse the resistance effect of EGFR-TKI resistant cell line A549. The relationship between EGFR/AKT signaling pathway and the mTOR signaling pathway and the mechanism in non-small cell lung cancer need further study.