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Gallic acid: prospects and molecular mechanisms of its anticancer activity

Subramanian, Aruna Priyadarshini and John, Agnes Aruna and Vellayappan, Muthu Vignesh Ignesh and Balaji, Arunpandian and Jaganathan, Saravana Kumar and Supriyanto, Eko and Yusof, Mustafa (2015) Gallic acid: prospects and molecular mechanisms of its anticancer activity. RSC Advances, 5 (45). pp. 35608-35621. ISSN 2046-2069

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Official URL: http://dx.doi.org/10.1039/c5ra02727f


Cancer is the second leading cause of death worldwide. There is always a huge demand for novel anticancer drugs and scientists explore various natural and artificial compounds to overcome this. Gallic acid (GA) is one of the phenolic acids found in many dietary substances and herbs used in ancient medicine. It possesses antiinflammatory, antioxidant, antiviral and antibacterial properties. The present review summarizes the anticancer activity of GA and its derivatives. Various in vitro and in vivo experiments of GA against a variety of cancer cell lines were reported. The previous studies show that the anticancer activity of GA is related to the induction of apoptosis through different mechanisms like generation of reactive oxygen species (ROS), regulation of apoptotic and anti-apoptotic proteins, suppression and promotion of oncogenes, inhibition of matrix metalloproteinases (MMPs) and cell cycle arrest depending upon the type of cancer investigated. Conclusively, GA and its derivatives may be considered as a potent drug for cancer treatment alone as well as in combination with other anticancer drugs to increase the efficiency of chemotherapy. However, there is still a need for more experimentation in knock-out animal models and human clinical trials to promote and place GA and its derivatives on the commercial market

Item Type:Article
Uncontrolled Keywords:cell culture, cell death, chemotherapy, oncogenic viruses
Subjects:R Medicine > R Medicine (General)
Divisions:Biosciences and Medical Engineering
ID Code:55452
Deposited By: Fazli Masari
Deposited On:08 Sep 2016 06:04
Last Modified:15 Feb 2017 04:59

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