Effect of silencing FGL1 on sensitivity of gefitinib in lung adenocarcinoma cells

Acta Universitatis Medicinalis Anhui 2020 06 v.55 854-859     font:big middle small

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Authors:Gao Weiwei; Sun Cuilan; Hao Jiqing

Keywords:lung adenocarcinoma;fibrinogen-like protein 1;EGFR-TKIs resistance;gefitinib sensitivity

DOI:10.19405/j.cnki.issn1000-1492.2020.06.007

〔Abstract〕 Objective To investigate the effect of silenced fibrin original protein 1(FGL1) on the drug sensitivity of gefitinib in lung adenocarcinoma cells. Methods Real-time quantitative PCR and Western blot were used to detect the differential expression of FGL1 in lung adenocarcinoma gefitinib-sensitive cell line PC9 and gefitinib-resistant cell line PC9/GR. FGL1 expression was silenced in gefitinib resistant strain PC9/GR. CCK-8 assay was used to detect cell proliferation in each group. Flow cytometry was used to determine the apoptosis rate of each group. Western blot was used to determine relative expression levels of apoptotic proteins Bcl-2, Bax, Caspase-3 and Cleaved-Caspase-3. Results FGL1 was highly expressed in PC9/GR cells. Silencing FGL1 inhibited the proliferation of PC9/GR and increased the apoptosis rate of PC9/GR cells(P<0.05). Western blot showed no significant difference in the expression of Caspase-3 in each group(P>0.05). Compared with the control group, the expression of Bax and Bcl-2 in gefitinib group showed no significant difference, while the expression of Cleaved-Caspase-3 was up-regulated, with statistically significant difference(P<0.05). After FGL1 was silenced, Bcl-2 protein expression was down-regulated, while Bax and Cleaved-Caspase-3 protein expression was up-regulated, with statistically significant differences(P<0.05). Conclusion Silencing FGL1 can inscrease the sensitivity of lung adenocarcinoma cells to gefitinib, inhibit cell proliferation, promote cell apoptosis, and provide potential therapeutic targets for gefitinib resistant lung adenocarcinoma patients.