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.
journal_name
FEBS Open Biojournal_title
FEBS open bioauthors
Yan H,Tian R,Wang W,Zhang M,Wu J,He Jdoi
10.1002/2211-5463.12364subject
Has Abstractpub_date
2018-01-26 00:00:00pages
332-338issue
3issn
2211-5463pii
FEB412364journal_volume
8pub_type
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