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PLEK2 functions as a co-factor of YTHDF2 to enhance TYMS mRNA stability in colorectal cancer

ABSTRACT: High expression of nucleotide synthetic enzyme thymidylate synthase (TYMS) is responsible for the resistance to fluorouracil (FU) treatment and worse survival in colorectal cancer. Herein, we revealed that Pleckstrin-2 (PLEK2), highly expressed in CRC, enhanced TYMS mRNA stability via its interaction with YTHDF2 in a m6A-dependent manner. Silencing of PLEK2 led to the downregulation of TYMS, and consequent inhibition of CRC cell proliferation via the cellular senescence. Additionally, PLEK2 is also required for CRC cell migration, invasion and stemness-like properties. PLEK2 inhibition is sufficient to ameliorate the progression of CRC. Moreover, loss of PLEK2 inhibited AOM/DSS-induced colonic tumorigenesis in vivo. Together, our study identified PLEK2 as a key regulator for the progress of CRC via the regulation of TYMS expression, and demonstrated that PLEK2 is a novel therapeutic target for CRC.

ORGANISM(S): Homo sapiens

PROVIDER: GSE252234 | GEO | 2025/07/23

REPOSITORIES: GEO

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PLEK2 functions as a co-factor of YTHDF2 to enhance TYMS mRNA stability in colorectal cancer

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