Published online May 15, 2020. doi: 10.4251/wjgo.v12.i5.514
Peer-review started: December 17, 2019
First decision: February 20, 2020
Revised: March 18, 2020
Accepted: March 28, 2020
Article in press: March 28, 2020
Published online: May 15, 2020
Processing time: 149 Days and 0.3 Hours
Colorectal cancer (CRC) is a worldwide problem, which has been associated with changes in diet and lifestyle pattern. As a result of colonic fermentation of dietary fibres, short chain free fatty acids are generated which activate free fatty acid receptors (FFAR) 2 and 3. FFAR2 and FFAR3 genes are abundantly expressed in colonic epithelium and play an important role in the metabolic homeostasis of colonic epithelial cells. Earlier studies point to the involvement of FFAR2 in colorectal carcinogenesis.
To understand the role of short chain FFARs in CRC.
Transcriptome analysis console software was used to analyse microarray data from CRC patients and cell lines. We employed short-hairpin RNA mediated down regulation of FFAR2 and FFAR3 genes, which was validated using quantitative real time polymerase chain reaction. Assays for glucose uptake and cyclic adenosine monophosphate (cAMP) generation was done along with immunofluorescence studies to study the effects of FFAR2/FFAR3 knockdown. For measuring cell proliferation, we employed real time electrical impedance-based assay available from xCELLigence.
Microarray data analysis of CRC patient samples showed a significant down regulation of FFAR2 gene expression. This prompted us to study the FFAR2 in CRC. Since, FFAR3 shares significant structural and functional homology with FFAR2, we knocked down both these receptors in CRC cell line HCT 116. These modified cell lines exhibited higher proliferation rate and were found to have increased glucose uptake as well as increased level of glucose transporter 1. Since, FFAR2 and FFAR3 signal through G protein subunit (Gαi), knockdown of these receptors was associated with increased cAMP. Inhibition of protein kinase A (PKA) did not alter the growth and proliferation of these cells indicating a mechanism independent of cAMP/PKA pathway.
Our results suggest role of FFAR2/FFAR3 genes in increased proliferation of colon cancer cells via enhanced glucose uptake and exclude the role of PKA mediated cAMP signalling. Alternate pathways could be involved that would ultimately result in increased cell proliferation as a result of down regulated FFAR2/FFAR3 genes. This study paves the way to understand the mechanism of action of short chain FFARs in CRC.
Core tip: Free fatty acid receptors (FFAR) have been reported to be associated with colorectal cancer (CRC). In this report, we studied short chain FFAR2 and FFAR3 and have provided preliminary evidence about the possible involvement of increased glucose uptake in FFAR2 and FFAR3 knockdown clones of CRC cell line. We generated double knock down for FFAR2 and FFAR3 genes in a CRC cell line (HCT116) and studied possible mechanisms of increased cell proliferation in these cells.