Suppression of EGFR-STAT3 signaling inhibits tumorigenesis in a lung cancer cell line

摘要

Overactive epidermal growth factor receptor (EGFR) signaling often underlies the rapid expansion of cancerous tissue. EGFR signaling is mediated by transcription factor signal transducer and activator of transcription 3, or STAT3. This study sought to investigate the effects of altered EGFR/STAT3 signal transduction on lung cancer cells in vitro. Lung cancer cells from the cell line A549 were divided into test and control groups. Test group cells were treated with an EGFR monoclonal antibody, Nimotuzumab, while control cells received no treatment. EGFR and STAT3 protein expression, cell apoptosis rate, cell proliferation, cell invasion, and cell division were analyzed and compared. Compared to cells in the control group, lung cancer cells treated with Nimotuzumab showed slowed proliferation rates, accelerated apoptosis, decreased invasion, and arrested cell division (emP/em < 0.05). In conclusion, altered EGFR/STAT3 signaling results in significant changes in the biology of lung cancer cells.