Impact of coconut kernel extract on carcinogen-induced skin cancer model: Oxidative stress, C-MYC proto-oncogene and tumor formation

Sorra Sandhya; Joyeeta Talukdar; Gayatri Gogoi; Kumar Saurav Dey; Bikul Das; Debabrat Baishya

doi:10.1016/j.heliyon.2024.e29385

Impact of coconut kernel extract on carcinogen-induced skin cancer model: Oxidative stress, C-MYC proto-oncogene and tumor formation

Heliyon. 2024 Apr 16;10(8):e29385. doi: 10.1016/j.heliyon.2024.e29385. eCollection 2024 Apr 30.

Authors

Sorra Sandhya^{1

2}, Joyeeta Talukdar^{1

2}, Gayatri Gogoi³, Kumar Saurav Dey⁴, Bikul Das^{2

5}, Debabrat Baishya¹

Affiliations

¹ Department of Bioengineering and Technology, Gauhati University, Guwahati, Assam, India.
² Department of Cancer and Stem Cell Biology, KaviKrishna Laboratory, Indian Institute of Technology-Guwahati Research Park, Assam, India.
³ Department of Pathology, Assam Medical College and Hospital (AMCH), Assam, India.
⁴ Guwahati Biotech Park, Guwahati, Assam, India.
⁵ Department of Stem Cell and Infection, Thoreau Lab for Global Health, University of Massachusetts, Lowell, MA, USA.

Abstract

This study aimed at analysing the effects of coconut (Cocos nucifera L.) kernel extract (CKE) on oxidative stress, C-MYC proto-oncogene, and tumour formation in a skin cancer model. Tumorigenesis was induced by dimethylbenz[a]anthracene (DMBA)/12-O-tetradecanoylphorbol-13-acetate (TPA). In vitro antioxidant activity of CKE was assessed using 2, 2-diphenyl-1-picrylhydrazyl (DPPH), hydrogen peroxide (H₂O₂), total phenolic and flavonoid content assays. CKE showed a higher antioxidant activity then ascorbic acid (*P < 0.05, ****P < 0.0001). HPLC and NMR study of the CKE revealed the presence of lauric acid (LA). Following the characterization of CKE, mice were randomly assigned to receive DMBA/TPA Induction and CKE treatment at different doses (50, 100, and 200 mg/kg) of body weight. LA 100 mg/kg of body weight used as standard. Significantly, the CKE200 and control groups' mice did not develop tumors; however, the CKE100 and CKE50 treated groups did develop tumors less frequently than the DMBA/TPA-treated mice. Histopathological analysis revealed that the epidermal layer in DMBA-induced mice was thicker and had squamous pearls along with a hyperplasia/dysplasia lesion, indicating skin squamous cell carcinoma (SCC), whereas the epidermal layers in CKE200-treated and control mice were normal. Additionally, the CKE treatment demonstrated a significant stimulatory effect on the activities of reactive oxygen species (ROS), glutathione (GSH), catalase (CAT), and superoxide dismutase (SOD), as well as an inhibitory effect on lipid peroxidase (*P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001) and c-MYC protein expression (*P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001). In conclusion, CKE prevents the growth of tumors on mouse skin by reducing oxidative stress and suppressing c-MYC overexpression brought on by DMBA/TPA induction. This makes it an effective dietary antioxidant with anti-tumor properties.

Keywords: Coconut karnel extract (CKE); DMBA/TPA; Oxidative stress; Skin squamous cell carcinoma (SCC); c-MYC gene.