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Transcriptome analysis of HCT116 cells subjected to low glucose or depleted of MAPKAPK2 expression.

GSE291324 Homo sapiens Expression profiling by high throughput sequencing 8 samples Submitted 2026/02/06 Platform GPL34284
Summary
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.
Published in
Metabolic stress conditions dictate MAPKAPK2-dependent efficiency of MEK1/2 inhibition in colorectal carcinoma
Kumari N, Chen X, Baldwin AM et al. · Proceedings of the National Academy of Sciences of the United States of America 2026 · PMID 41662531 · doi:10.1073/pnas.2505331123
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Also filed as BioProject PRJNA1232821 and SRA study SRP568525. Searching any of these in the dataset finder brings you back here.

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