English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Zendy Plus

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Zendy Tools

Zendy Open

Colorectal cancer represents one of the most challenging diseases. Increasingevidence indicates that aberrant expression of microRNAs (miRNAs) is related topathogenesis of colorectal cancer. Cancer cells reprogram metabolic pathways tosustain higher proliferation rates. Whether mechanisms underlying the role ofmiRNA in colorectal cancer are involved in metabolic reprogramming and the mechanismsthrough which miRNAs alter cancer metabolism are as yet unknown. Herein, we showthat miR-124, miR-137 and miR-340 are associated with poor prognosis of colorectalcancer. Expression of these miRNAs inhibits the growth of colorectal cancer cells.PKM (pyruvate kinase isozyme) alternative splicing proteins (PTB1/hnRNAPA1/hnRNAPA2),which control the inclusion of exon 9 (PKM1) or exon 10 (PKM2), are targeted bymiR-124, miR-137 and miR-340. Consequently, miR-124, miR-137 and miR-340 switchPKM gene expression from PKM2 to PKM1. High ratios of PKM1/PKM2 inhibit the glycolysisrate, but elevate the glucose flux into oxidative phosphorylation. These resultsdemonstrate that miRNAs (miR-124, miR-137 and miR-340) impair colorectal cancergrowth by counteracting the Warburg effect due to regulating alternative splicingof the PKM gene.

miR-124, miR-137 and miR-340 regulate colorectal cancer growth via inhibition of the Warburg effect