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. 2019 Mar-Apr;24(2):549-554.

Root extract of Prunella vulgaris inhibits in vitro and in vivo carcinogenesis in MCF-5 human breast carcinoma via suppression of angiogenesis, induction of apoptosis, cell cycle arrest and modulation of PI3K/AKT signalling pathway

Affiliations
  • PMID: 31128004
Free article

Root extract of Prunella vulgaris inhibits in vitro and in vivo carcinogenesis in MCF-5 human breast carcinoma via suppression of angiogenesis, induction of apoptosis, cell cycle arrest and modulation of PI3K/AKT signalling pathway

Wei Gao et al. J BUON. 2019 Mar-Apr.
Free article

Abstract

Purpose: In this study we examined the anticancer effects of methanolic root extract of Prunella Vulgaris (PVE) against the MCF-5 breast cancer (BC) cell line along with its mode of action.

Methods: The proliferation rate of the MCF-5 cells was assessed by MTT assay. Apoptosis was confirmed by acridine orange (AO)/ethidium bromide (EB) and annexin V/propidium iodide (PI) staining. DNA damage was checked by comet assay. Cell cycle analysis was performed by flow cytometry. Protein expression was determined by western blotting. In vivo evaluation of the extract was carried out in xenografted tumor mice models.

Results: PVE inhibited the growth of the MCF-5 cells and exhibited an IC50 value of 25 µg/ml. The investigation of underlying mechanism revealed that PVE triggered apoptotic cell death of the MCF-5 cells which was also associated with enhancement of the expression of Bax and decrease in the expression of Bcl-2. PVE also caused arrest of the cells in the G2/M phase of the cell cycle and also exerted the anti-angiogenic effects. In vivo evaluation of PVE showed that it could inhibit the tumor weight and volume, suggestive of the anticancer potential of PVE.

Conclusion: The root extract of Prunella vulgaris in this study was shown to exert potent anticancer effects in MCF-7 human BC cells both in vitro and in vivo, accompanied with apoptosis induction, inhibition of angiogenesis, cell cycle arrest, and modulation of PI3K/AKT signaling pathway.

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