Abstract

Thymoquinone is an anticancer phytochemical commonly found in black cumin. In this review, we discuss the potential of thymoquinone as anticancer molecule, its mechanism of action and future usage in clinical applications. Thymoquinone exhibits anticancer activity via numerous mechanisms of action, specifically by showing selective antioxidant and oxidant activity, interfering with DNA structure, affecting carcinogenic signaling molecules/pathways and immunomodulation. In vitro activity of thymoquinone has been further implicated in animal models of cancer; however, no clinical application has been proven yet. This is the optimum time to focus on clinical trials for developing thymoquinone as a future drug in cancer therapeutics.

Highlights

  • Every year, millions of people are diagnosed with cancer, which is the second leading cause of death worldwide after myocardial infarction

  • Both seeds and oil from Nigella sativa plants are used in medicinal purposes, and they are known for their anticancer, antidiabetic, antihypertensive, antimicrobial, analgesic, immunomodulatory, anti-inflammatory, spasmolytic, hepato-protective, renal-protective, gastroprotective, bronchodilative and antioxidant activities [4,5,6]

  • In mouse model of familial adenomatous polyposis (FAP), thymoquinone interfered with polyp progression by inducting tumor-cell specific apoptosis and by modulating Wnt signaling through the activation of GSK-3β, reducing the risk of colorectal cancer [63]

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Summary

Introduction

Millions of people are diagnosed with cancer, which is the second leading cause of death worldwide after myocardial infarction. In human colon cancer cells (HCT116), thymoquinone induced apoptosis, which was associated with the up-regulation of Bax and the inhibition of Bcl-2 as well as the activation of caspases -9, -7 and -3 and the induction of the cleavage of poly-(ADP-ribose) polymerase (PARP) [25]. In breast cancer cell lines (MDA-MB-468 and T47D), thymoquinone interfered with PI3K/Akt signaling and promoted G(1) arrest and induced apoptosis [27].

Results
Conclusion
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