Effect of Erlotinib Combined with Radiotherapy on Proliferation and Apoptosis of Human Non-Small Cell Lung Cancer Cells and its Possible Mechanism Exploration.

To explore the effects and possible mechanisms of erlotinib combined with radiotherapy on the proliferation and apoptosis of human non-small cell lung cancer cells. Blank control group, non-small cell lung cancer group and erlotinib group were set cells in the blank control group were human bronchial epithelioid cells without any treatment and cultured routinely. The proliferation ability of the cells in the three groups was detected by cell counting kit-8, Western blot was used to assess protein expression, quantitative polymerase chain reaction was used to measure messenger ribonucleic acid expression, and Transwell was used to determine metastatic potential. The quantity of migrating cells and the rate of cell growth of non-small cell lung cancer group were higher than that of blank control group; the cell metastasis activity number of erlotinib group were reduced than that of non-small cell lung cancer group. The cell invasion number of non-small cell lung cancer group was higher than blank control group; erlotinib group was reduced than that of non-small cell lung cancer group. The overall apoptosis rate was higher than the non-small cell lung cancer group. The apoptotic proteins Fas, B-cell lymphoma 2-associated X protein and Fas ligand were higher in the erlotinib group than in the non-small cell lung cancer group, and the B-cell lymphoma 2 was reduced than the nonsmall cell lung cancer group. The 5' adenosine monophosphate-activated protein kinase and peroxisome proliferator-activated receptor coactivator-1 alpha in the non-small cell lung cancer group were reduced than the blank control group and erlotinib group were higher than the non-small cell lung cancer group. The protein mitogen-activated protein kinase and peroxisome proliferator-activated receptor coactivator-1 alpha in the non-small cell lung cancer group were reduced than the blank control group and erlotinib group were higher than those in the non-small cell lung cancer group. The mechanism of erlotinib’s capacity to lower the viability of non-small cell lung cancer cells, block their proliferation, migration, and invasion ability, and induce apoptosis may be connected to the control of the 5' adenosine monophosphate-activated protein kinase/ peroxisome proliferator-activated receptor coactivator-1 alpha signaling pathway. [ABSTRACT FROM AUTHOR]