Transcriptome analysis of HCT116 cells subjected to low glucose or depleted of MAPKAPK2 expression.
MAPKAPK2, a component of p38 signaling pathway, is upregulated in colorectal cancer (CRC) and is known to regulate glucose metabolism. Utilizing HCT116, a CRC cell line, we identified that cancer cells can withstand low glucose conditions via upregulation of stress-induced survival pathways and downregulation of DNA metabolism and cell cycle related genes. As p38/MAPKAPK2 signaling is a well-known stress activated pathway, understanding the role played by this pathway in glucose-deprivation conditions was of particular interest. Interestingly, MAPKAPK2 levels decline in low glucose. We observed that MAPKAPK2 depletion results in upregulation or downregulation of pathways similar to glucose deprivation. Our findings suggest that MAPKAPK2 abundance plays critical role in proliferation versus survival depending on glucose availability. Overall design: HCT116 cells expressing control shRNA were cultured in DMEM with or without glucose (20 mM vs 0 mM glucose) for 24 hours, followed by RNA extraction and RNA-sequencing.  HCT116 cells expressing control and MAPKAPK2 targeting shRNAs were also subjected to RNA-sequecing.