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Aberrant Ki-67 expression through 3'UTR alternative polyadenylation in breast cancers.


ABSTRACT: Ki-67 (MKI67) is a marker of cellular proliferation of cancer. Here, we show that Ki-67 is post-transcriptionally regulated through alternative polyadenylation (APA) and microRNAs in breast cancer. We show that shortening of the Ki-67 3'UTR results in the loss of the binding sites for the suppressive miRNAs and thus renders the transcript with a shortened 3'UTR insusceptible to miRNA-mediated suppression. This APA-mediated shortening of the Ki-67 3'UTR contributes to increased mRNA stability and enhanced translational efficiency. In summary, our results not only highlight the post-transcriptional regulation of Ki-67 involving APA and microRNAs but also suggest that Ki-67 3'UTR disruption could serve as a molecular marker in breast cancer.

SUBMITTER: Yan H 

PROVIDER: S-EPMC5832968 | biostudies-literature | 2018 Mar

REPOSITORIES: biostudies-literature

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Aberrant <i>Ki-67</i> expression through 3'UTR alternative polyadenylation in breast cancers.

Yan Hong H   Tian Rui R   Wang Wei W   Zhang Min M   Wu Jing J   He Jie J  

FEBS open bio 20180126 3


Ki-67 (MKI67) is a marker of cellular proliferation of cancer. Here, we show that Ki-67 is post-transcriptionally regulated through alternative polyadenylation (APA) and microRNAs in breast cancer. We show that shortening of the <i>Ki-67</i> 3'UTR results in the loss of the binding sites for the suppressive miRNAs and thus renders the transcript with a shortened 3'UTR insusceptible to miRNA-mediated suppression. This APA-mediated shortening of the <i>Ki-67</i> 3'UTR contributes to increased mRNA  ...[more]

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