International Journal of Cancer Research1811-97271811-9735Academic Journals Inc.10.3923/ijcr.2019.17.22Al MahriSaeed Al GhamdiAmal MohammadSameer Azhar AzizMohammad 12019151Background and Objective: Short chain free fatty acids (SCFAs) like butyrate, propionate and acetate are produced by microbiota in the gut. SCFAs have been shown to exert their metabolic effects through their cognate receptors (FFAR2 and FFAR3). These receptors are abundantly expressed in colonic epithelium and several studies have shown that these receptors play an important role in the metabolic homeostasis of colonic epithelial cells and are possibly involved in colorectal carcinogenesis. This study was initiated to understand the role of FFAR3 gene in colorectal cancer cell growth and proliferation. Materials and Methods: The HCT116 colorectal cancer cell line was engineered to develop stable FFAR3 knockdown using shRNA mediated gene silencing technology. Down regulation of FFAR3 mRNA was confirmed by RT-PCR and consequences of FFAR3 down regulation on cell growth and proliferation were analyzed. Results: The data revealed that FFAR3 down regulation had no impact on proliferation and growth rate of engineered HCT116 cells. Moreover, FFAR3 knockdown cells did not show any difference in the glucose uptake rate or cyclic adenosine monophosphate (cAMP) levels as compared to control cells. The most likely explanation of lack of FFAR3 effect on HCT116 cell metabolism was that FFAR2 compensated for the loss of FFAR3 and maintained the functionality of SCFAs. Conclusion: This study showed that FFAR3 gene alone does not impact growth and cell proliferation of colorectal cancers. Further studies are needed to fully understand the role of FFAR3 by using double knockdown cells (FFAR2/FFAR3).]]>Azcarate-Peril, M.A., M. Sikes and J.M. Bruno-Barcena,2011301G401G424Aziz, M.A., Z. Yousef, A.M. Saleh, S. Mohammad and B. Al Knawy,20171187078Cummings, J.H. and G.T. Macfarlane,199721357365Russell, W.R., L. Hoyles, H.J. Flint and M.E. Dumas,201316246254Young, G.P.,199654447Matthews, G.M., G.S. Howarth and R.N. Butler,2007610511057Gui, H. and Z. Shen,20169966276638Piazzi, G., G. D'argenio, A. Prossomariti, V. Lembo and G. Mazzone et al.,201413520042013Le Poul, E., C. Loison, S. Struyf, J.Y. Springael and V. Lannoy et al.,20032782548125489Karaki, S.I., H. Tazoe, H. Hayashi, H. Kashiwabara, K. Tooyama, Y. Suzuki and A. Kuwahara,200839135142Tazoe, H., Y. Otomo, I. Kaji, R. Tanaka, S.I. Karaki and A. Kuwahara,200859251262Kim, M.H., S.G. Kang, J.H. Park, M. Yanagisawa and C.H. Kim,2013145396406Pan, P., K. Oshima, Y.W. Huang, K.A. Agle and W.R. Drobyski et al.,2018143886896Nohr, M.K., M.H. Pedersen, A. Gille, K.L. Egerod and M.S. Engelstoft et al.,201315435523564Ang, Z., D. Xiong, M. Wu and J.L. Ding,201732289303Iguchi, H., T. Mitsui, M. Ishida, S. Kanba and J. Arita,201158747759Vitali, E., V. Cambiaghi, A. Spada, A. Tresoldi and A. Zerbi et al.,2015339241251Sirotkin, A.V., A. Benco, A. Tandlmajerova, M. Laukova and D. Vasicek et al.,20183011451153Maddalena, F., G. Lettini, R. Gallicchio, L. Sisinni and V. Simeon et al.,201514490498Moon, S.H., S.J. Lee, K.H. Jung, C.H.T. Quach and J.W. Park et al.,201618F-FDG by suppressing mitochondrial respiration and augments sensitivity to glucose restriction.]]>57129135Zhang, R., J. Li, X. Yan, K. Jin and W. Li et al.,20172017Eldai, H., S. Periyasamy, S. Al Qarni, M. Al Rodayyan and S.M. Mustafa et al.,20132013Aziz, M.A., S. Periyasamy, Z. Al Yousef, I. AlAbdulkarim, M. Al Otaibi, A. Alfahed and G. Alasiri,20142014Aziz, M.A., S. Periyasamy, Z. Yousef, A. Deeb and M. AlOtaibi,201422931