Ethanolic Extract of Moringa oleifera L. Increases Sensitivity of WiDr Colon Cancer Cell Line Towards 5-Fluorouracil

Kholid Alfan Nur, Herwandhani Putri, Fany Mutia Cahyani, Aulia Katarina, Ratna Asmah Susidarti, Edy Meiyanto


For more than four decades, combination chemotherapy (co-chemotherapy) has been employed as a means to increase the effectiveness of chemotherapy regiments. The aim of our research is to investigate the activity of Moringa oleifera L. (tanaman kelor) ethanolic extract (MEE) as a co-chemotherapy agent with 5-fluorouracil (5-FU) on WiDr colon cancer cell line. Evaluation of MEE potency as a co-chemotherapy agent with 5-FU was based on cytotoxic activity based on percent cell viability via MTT assay, and based on apoptosis observation via the double staining method using acrydin orange – ethidium bromide (AE) as the staining reagent.Cytotoxicity evaluation of single treatment using concentrations of 5, 20, 50, 100,125, and 250 µg/ml of MEE reduced cell viability 24 hours post-treatment. 5, 50, and 250 µg/ml of MEE was chosen as the combination concentrations with 1000 µM 5-FU. MTT assay 24 hours and 48 hours post-combination treatment showed significant cell viability reduction in comparison to those of single treatments. Apoptosis observation using the double staining method shows the presence of apoptotic cells 48 hours post combination treatment. MEE is a potential co-chemotherapy agent by increasing the sensitivity of WiDr colon cancer cell line towards 5-FU.

Keywords: co-chemotherapy, 5-fluorouracil, Moringa oleifera L., colon cancer

Full Text:



Bharali, R., Tabassum, J., and Azad, M.R.H., 2003, Chemomodulatory effect of Moringa Oleifera L. on hepatic carcinogen metabolising enzyme, antioxidant parameters, and skin papillomagenesis in mice, Asia Pacific Journal of Cancer Prevention, 4: 131 – 139.

Brenner, D.E., 2002, New paradigms in oncological therapeutics: redefining combination chemotherapy, Annals of Oncology, 13: 1697 – 1698.

De Angelis, P.M., Svendsurd, D.H., Kravik, K.L., and Stokke, T., 2006, Cellular response to fluorouracil (5-FU) in FU-resistant colon cancer cell lines during treatment and recovery, Mol. Cancer, 5: 20.

Hetch, S.S., 2009, Chemoprevention of cancer by isothicyanates, modifiers of carcinogen metabolism, Journal of Nutrition, 129: 768s – 774s.

Kodach, L.L., Bos, C.L., Duran, N., Peppelenbosch, M.P., Ferreira, C.V., and Hardwick, J.C.H., 2006, Violacein synergistically increases 5-fluorouracil cytotoxicity, induces apoptosis, and inhibits Akt-mediated signal transduction in human colorectal cancer cells, Carcinogenesis, 27(3): 508-516.

Lee, J.W., and Cho, M.K., 2008, Phenethyl Isothiocyanates induced apoptosis via down regulation of Bcl-2/XIAP and triggering the mitochondrial pathway in MCF-7 cells, Arch. Pharm. Res., 31(12): 1604-1612.

Srivastava, S.K., and Singh, S.V., 2004, Cell cycle arrest, apoptosis induction and inhibition of nuclear factor kappa B activation in antiproliverative activity of benzyl isothiocyanate against human pancreatic cancer cells, Carcinogenesis, 25(9): 1701-1709.

Zhang, R., Loganathan, S., Humphreys, I., and Srivastava, S., 2009, Benzyl isothiocyanate-induced DNA damage causes G2/M cell cycle arrest and apoptosis in human pancreatic cancer cells, Journals of Nutrition, 136: 2728-2734.


Copyright (c) 2017 Indonesian Journal of Cancer Chemoprevention

Indexed by:




Indonesian Society for Cancer Chemoprevention