Quinic acid attenuates oral cancer cell proliferation by downregulating cyclin D1 Expression and Akt signaling

Articles

Abstract
Pharmacognosy Magazine,2018,14,55s,s14-s19.
Published:June 2018
Type:Original Article
Authors:
Author(s) affiliations:

Anjana Singh1, Shyam Singh Chauhan2, Vishwas Tripathi1
1 School of Biotechnology, Gautam Buddha University, Greater Noida, India
2 Department of Biochemistry, All India Institute of Medical Sciences, New Delhi, India

Abstract:

Background: Quinic acid (QA), a natural compound found in fruits, for example in apple, berries, and coffee beans, is a neutraceutical chiral compound used to synthesize new pharmaceutically important chemical compounds. Platinum-based drugs such as cisplatin are widely used in the therapy, including oral cancer, one of the most prevalent cancer. Due to their severe side effects and acquired resistance to the treatment, phytotherapies are being explored to find out strong anticancer compounds that can alone and synergistically prevent and cure cancer without side effects. Objective: This study aimed to find out the mechanism behind the anticancer property of QA, a natural compound alone and synergistically with cisplatin in oral cancer cells (squamous cell carcinoma-4 [SCC-4]). Materials and Methods: Oral cancer cells were treated with QA alone and synergistically with cisplatin. MTT assay was performed to investigate the cytotoxic effect of QA and QA + cisplatin combination. Apoptotic effects of QA and QA + cisplatin combination were analyzed using DAPI and real-time-polymerase chain reaction for the expression of apoptotic marker genes. Effect of QA and QA + cisplatin combination was assessed by flow cytometry and immunoblotting technique. Results: Our result shows that QA promotes apoptosis in oral cancer cells by downregulating the expression of anti-apoptotic genes and attenuating the expression of cyclin D1 and Akt signaling pathway. Moreover, QA shows synergistic effect with cisplatin in these cells. Conclusion: QA inhibits cell proliferation and promotes apoptosis in oral cancer cells (SCC-4) alone and with cisplatin.

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