西亚试剂：CFIm25 1inks alternative polyadenylation to glioblastoma tu

发布时间：2025-08-14

Chioniso P. Masamha, Zheng Xia, Jingxuan Yang, Todd R. Albrecht, Min Li, Ann-Bin Shyu,Wei Li & Eric J. Wagner

The global shortening of messenger RNAs through alternative polyadenylation (APA) that occurs during enhanced cellular proliferation represents an imp0rtant, yet poorly understood mechanism of regulated gene expressi0n1, 2. The 3′ untranslated region (UTR) truncation of growth-promoting mRNA transcr-pts that relieves intrinsic microRNA- and AU-rich-element-mediated repression has been observed to correlate with cellular transformation3; however, the imp0rtance to tumorigenicity of RNA 3′-end-processing factors that potentially govern APA is unknown. Here we identify CFIm25 as a broad repressor of proximal poly(A) site usage that, when depleted, increases cell proliferation. Applying a regression model on standard RNA-sequencing data for novel APA events, we identified at least 1,450 genes with shortened 3′ UTRs after CFIm25 knockdown, representing 11% of significantly expressed mRNAs in human cells. Marked increases in the expressi0n of several known oncogenes, including cyclin D1, are observed as a consequence of CFIm25 depletion. imp0rtantly, we identified a subset of CFIm25-regulated APA genes with shortened 3′ UTRs in glioblastoma tumours that have reduced CFIm25 expressi0n. Downregulation of CFIm25 expressi0n in glioblastoma cells enhances their tumorigenic properties and increases tumour size, whereas CFIm25 overexpressi0n reduces these properties and inhibits tumour growth. These findings identify a pivotal role of CFIm25 in governing APA and reveal a previously unknown connection between CFIm25 and glioblastoma tumorigenicity.

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