Found programs: National Natural Science Foundation of China (Nos. 81160447,81760878);Scientific Research Project of Jiangxi Provincial Department of Education (No.GJJ2200919);Natural Science Foundation of Jiangxi Province (Nos.20202BAB206073,20212BAB216066);Graduate Student Innovation and Entrepreneurship Training Project of Jiangxi Province (Nos.S202210412069,S202310412056);Science and Technology Innovation Team of Jiangxi University of Chinese Medicine (No.CXTD22013)
Authors:Zhan Xiaoxuan; Liu Chengyi; Peng Jiahua; Liu Shuzhen; Li Xin; Ren Yunying; Chen Danni; Li Peishuang; Liang Ruining
Keywords:cinnamaldehyde;RPS7;endometriosis;proliferation;migration;invasion;apoptosis
DOI:10.19405/j.cnki.issn1000-1492.2025.03.004
〔Abstract〕 Objective To investigate the effects of cinnamaldehyde(CA) on the growth, metastasis and apoptosis of human endometriosis(EMs) cells and to explore whether the mechanism is related to ribosomal protein S7(RPS7) expression. Methods Endometriosis cells were divided into control group, CA group, sh-NC group, CA+sh-RPS7 group. Effects of CA on cell growth in human endometriotic cells were determined using Cell Counting Kit-8(CCK-8) and colony formation assay. Effects of CA on cell metastasis were performed by motility assay and Transwell assay. Effects of CA on cell apoptosis were evaluated by Hoechst 33258 staining and flow cytometry. Meanwhile, the levels of PCNA, E-cadherin, Vimentin, Bax and Bcl-2 were evaluated using Western blot in human endometriotic cells with treatment CA. The expression of RPS7 was detected by qRT-PCR and Western blot assay. The RPS7 overexpression of human endometriotic cells was established by cell transfection. CA-mediated effects on cell proliferation and apoptosis were determined by CCK-8 assay and flow cytometry in human endometriotic cells with RPS7 overexpression. Results CA repressed cell growth as well as down-regulated PCNA. The half inhibitory concentration(IC50) value was 53.60 μmol/L after 24 h treatment, and colony formation rate was 25.32%. Additionally, CA inhibited metastasis which was associated with downregulated Vimentin and upregulated E-cadherin. The relative migration rates were 35% and 29% as well as invasion rate was 40%. Further, CA induced apoptosis by cell cycle G2/M phase arrest and cell apoptosis rate was 25.1%, which related to the up-regulation of of Bax and the down-regulation of Bcl-2. CA inhibited the expression of RPS7 and overexpression of RPS7 promoted cell proliferation and suppressed apoptosis in CA-mediated cells. Conclusion CA inhibits cell growth, metastasis, and induces cell apoptosis by downregulating the expression of RPS7.