Fund programs: National Natural Science Foundation of China (No. 82060540);Graduate Education Innovation Plan Project of Guangxi(No. JGY2024318)
Authors:Ma Beibei; Cheng Lianyu; Zhang Zhongwei; Ye Guangbin; Li Yanli Ling Bo
Keywords:solasonine; lung adenocarcinoma; H1299; apoptosis;migration; STAT3;
DOI:10.19405/j.cnki.issn1000-1492.2025.07.004
〔Abstract〕 Objective To investigate the effect of solasonine regulation of the STAT3 signaling pathway on the bio- logical behavior of lung adenocarcinoma cells.Methods H1299 cells were treated with 0. 125,0. 25,0. 5 and 0. 75 mmol /L solasonine,respectively.The proliferative activity of H1299 cells was detected by CCK-8.The mi- gration and invasion ability of H1299 cells were detected by scratch,Transwell migration and invasion assay.The apoptosis level of H1299 cells was detected by flow cytometry and Hoechest 33258 /PI double staining.The protein expression levels of STAT3,p-STAT3 ,Bcl-2 ,Bax ,Caspase-3 ,Cl-Caspase-3 ,Snail ,Slug ,N-cadherin and E- cadherin in H1299 cells were detected by Western blot assay.Results Solasonine at different concentrations sig- nificantly reduced the proliferation of H1299 cells (P<0. 05) .0. 125 and 0. 25 mmol /L solasonine promoted the apoptosis of H1299 cells (P<0. 05) and inhibited the migration and invasion of H1299 cells (P<0. 05) .Solaso- nine inhibited the expression of STAT3,p-STAT3 and Bcl-2 proteins,enhanced the expression of Bax,Caspase-3 and Cl-Caspase-3 proteins.Solasonine inhibited the activation of STAT3 in cells,reduced Snail and Slug protein expression levels,enhanced E-cadherin,reduced N-cadherin(P<0. 05) .Conclusion Solasonine can inhibit the activation of STAT3 ,activate the Bcl-2 /Bax / Caspase3 apoptosis pathway ,inhibit the continuous proliferation of lung adenocarcinoma H1299 cells,and promote the apoptosis of lung adenocarcinoma H1299 cells.Meanwhile,it can inhibit the activation of STAT3,reduce the expression of Snail / Slug protein,affect the EMT transformation of lung adenocarcinoma H1299 cells,and inhibit the migration and invasion of lung adenocarcinoma H1299 cells.