Effects of shikonin on proliferation, apoptosis and cell cycle of human esophageal

Zhao Li; Huang Jingrong; Gong Chengxian; Wang Yi; QU Yinzong; JI Chunyan; Yang Jianmei

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Effects of shikonin on proliferation, apoptosis and cell cycle of human esophageal

VernacularTitle:紫草素对人食管癌TE-1细胞增殖、凋亡和细胞周期的影响及其可能的
Author: ZHAO Li ^{1
,

2} ; HUANG Jingrong ^{1
,

2} ; GONG Chengxian ^{1
,

2} ; WANG Yi ^{1
,

2} ; QU Yinzong ^{1
,

2} ; JI Chunyan ^{1
,

2} ; YANG Jianmei ^{1
,

2}
Author Information

1. Department of Gastroenterology, Hubei Provincial Hospital of Integrated Chinese &
2. Western Medicine, Wuhan 430015, Hubei, China
Publication Type:Journal Article
Keywords: shikonin; esophageal cancer; TE-1 cell; proliferation; apoptosis; cell cycle; TRAP1/Akt/mTOR signaling pathway
From: Chinese Journal of Cancer Biotherapy 2020;27(8):889-894
CountryChina
Language:Chinese
Abstract: [Abstract] Objective: To observe the effects of shikonin on the proliferation, apoptosis and cell cycle of human esophageal carcinoma TE-1 cells, and to explore its mechanism. Methods: TE-1 cells were treated with different concentrations of shikonin (0, 1, 5, 10 µmol/L). MTT assay was used to detect cell proliferation at different time points (24, 48 and 72 h). After treatment with shikonin for 48 h, cell apoptosis in TE-1 cells of each group was observed with Hoechst 33258 fluorescence staining. Flow cytometry was used to detect apoptosis and cell cycle. The changes in expression of TRAP1/Akt/mTOR signaling pathway related proteins were detected by Western blotting. Results: Shikonin inhibited the proliferation of TE-1 cells in a time-dose-dependent manner (P<0.05 or P<0.01). Compared with the control group, shikonin significantly promoted the apoptosis of TE-1 cells (P<0.01), induced the G0/G1 phase block of TE-1 cells (P<0.05 or P<0.01), and reduced the expression levels of TRAP1, p-Akt and p-MTOR (P<0.05 or P<0.01). The above effects were all dose-dependent. Conclusion: Shikonin can significantly inhibit the proliferation of TE-1 cells in vitro, induce G0/G1 phase arrest and promote apoptosis, which may be closely related to the inhibition of TRAP1/Akt/mTOR signaling pathway.
Full text:20200809.pdf