Molecular Mechanisms of Thymoquinone as Anticancer Agent

Author:

Alhmied Fatma1,Alammar Ali2,Alsultan Bayan2,Alshehri Muruj2,Pottoo Faheem Hyder2

Affiliation:

1. College of Medicine, Imam Abdulrahman Bin Faisal University, P.O BOX 1982, Dammam 31441, Saudi Arabia

2. Department of Pharmacology, College of Clinical Pharmacy, Imam Abdulrahman Bin Faisal University, P.O BOX 1982, Dammam 31441, Saudi Arabia

Abstract

Thymoquinone (TQ), the bioactive constituent of Nigella Sativa seeds, is a well-known natural compound for the management of several types of cancers. The anti-cancer properties of thymoquinone are thought to be operated via intervening with various oncogenic pathways, prevention of inflammation and oxidative stress, inhibition of angiogenesis and metastasis, and induction of apoptosis, as well as up-regulation and down-regulation of specific tumor suppressor genes and tumor promoting genes, respectively. The proliferation of various tumor cells is inhibited by TQ via induction of cell cycle arrest, disruption of the microtubule organization, and downregulating cell survival protein expression. TQ induces G1 phase cell cycle arrest in human breast cancer, colon cancer and osteosarcoma cells through inhibiting the activation of cyclin E or cyclin D and up-regulating p27 and p21, a cyclin dependent kinase (Cdk) inhibitor. TQ concentration is a significant factor in targeting a particular cell cycle phase. While high concentration of TQ induces G2 phase arrest in human breast cancer (MCF-7) cells, low concentration causes S phase arrest. This review article provides mechanistic insights into the anticancer properties of thymoquinone.

Publisher

Bentham Science Publishers Ltd.

Subject

Organic Chemistry,Computer Science Applications,Drug Discovery,General Medicine

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