Studies on apoptosis induced by B-norcholesteryl benzimidazole compounds in HeLa cells
[Display omitted] •B-norcholesteryl Benzimidazole Compounds can change cervical cancer HeLa cell morphology and inhibit its proliferation, invasion and metastasis.•Furthermore, the compound can induce apoptosis of HeLa cells.•The compounds block HeLa cell proliferation in the early stage of DNA synt...
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Veröffentlicht in: | Steroids 2021-04, Vol.168, p.108802, Article 108802 |
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Sprache: | eng |
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•B-norcholesteryl Benzimidazole Compounds can change cervical cancer HeLa cell morphology and inhibit its proliferation, invasion and metastasis.•Furthermore, the compound can induce apoptosis of HeLa cells.•The compounds block HeLa cell proliferation in the early stage of DNA synthesis (G0/G1 phase) and causes the mitochondrial membrane potential Δψm collapse.•Compound 1 can improve the expression of p53 mRNA.•Compound 2 down-regulated the expression of p53 and p21 mRNA.•Compound 3 upgrade the expression of p21 and p53 mRNA.
Certain B-norcholesteryl benzimidazole compounds were found to mediate marked anti-tumor proliferative effects in vitro in our earlier study. Here, the mechanism of action of these anti-tumor effects was evaluated using HeLa human cervical cancer cells. Methods for detecting cell invasion and migration, Annexin V-PI double staining, cell cycle status, and mitochondrial membrane potential Δψm were employed. These compounds were confirmed to significantly inhibit the proliferation of HeLa cells in vitro. Compound 1 induced apoptosis in S phase, compound 2induced apoptosis in the G0/G1 phase and compound 3 induced late apoptosis in the G2/M phase. These compounds induced HeLa cell apoptosis through depolarization of mitochondrial membrane potential Δψm in a dose-dependent manner. B-norcholesteryl benzimidazole compounds induced morphological changes in HeLa cells and inhibited proliferation, invasion and metastasis. Apoptosis was promoted by mechanisms involving p21 and p53 in this cervical cancer cell line. |
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ISSN: | 0039-128X 1878-5867 1878-5867 |
DOI: | 10.1016/j.steroids.2021.108802 |