CDS‑1548 induces apoptosis in HeLa cells by activating caspase 3

Zhang,Yuanxin; Ge,Yakun; Shi,Wei; Hu,Chenming; Bai,Xu; Rong,Jimin; Yu,Ming

doi:10.3892/ol.2019.10511

CDS‑1548 induces apoptosis in HeLa cells by activating caspase 3

Authors:
- Yuanxin Zhang
- Yakun Ge
- Wei Shi
- Chenming Hu
- Xu Bai
- Jimin Rong
- Ming Yu
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Affiliations: College of Biology and Food Engineering, Jilin Institute of Chemical Technology, Jilin, Jilin 132022, P.R. China, Key Laboratory for Molecular Enzymology and Engineering of The Ministry of Education, School of Life Science, Jilin University, Changchun, Jilin 130012, P.R. China, The Center for Combinatorial Chemistry and Drug Discovery, College of Pharmacy, Jilin University, Changchun, Jilin 130012, P.R. China
Published online on: June 21, 2019 https://doi.org/10.3892/ol.2019.10511
Pages: 1881-1887
Copyright: © Zhang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Cervical cancer continues to be a threat to female health globally. In the present study, the potential anticancer activity of 2‑[2‑hydroxyl‑1‑(4‑methoxy phenyl) ethyl]‑3‑(4‑benzyloxy phenyl) isoindolin‑1‑one (CDS‑1548), was evaluated in HeLa cells. CDS‑1548 is an organic small‑molecule compound characterized by two chiral centers, with the nuclear parent 1H‑isoindolin‑1‑one. CDS‑1548 administration significantly elevated the transcriptional activity of p53 and its downstream target genes in a dose‑dependent manner. Additionally, CDS‑1548 treatment increased the expression levels of p53 and mouse double minute 2 homolog, as well as inducing apoptosis in HeLa cells. Furthermore, CDS‑1548 treatment downregulated the expression of B‑cell lymphoma 2, upregulated Bcl‑2 homologous antagonist killer, promoted the release of cytochrome c from mitochondria to cytoplasm, and activated the production of caspase 3 and 9. Collectively, these results suggested that CDS‑1548 inhibited HeLa cell proliferation by promoting G2/M cell cycle phase arrest and inducting of mitochondria‑mediated apoptosis.

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