Journal
CELL CYCLE
Volume 8, Issue 22, Pages 3648-3651Publisher
TAYLOR & FRANCIS INC
DOI: 10.4161/cc.8.22.9909
Keywords
E-cadherin; PSF; PTB-associated splicing factor; proliferation; tumor progression; RNA binding protein; oncogene
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Funding
- Secretaria Xeral I+D+I, Xunta de Galicia, Spain
- NIA-IRP, NIH
- Medical Research Council [MC_U122669938] Funding Source: researchfish
- MRC [MC_U122669938] Funding Source: UKRI
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Hakai, an E3 ubiquitin ligase for the E-cadherin complex, plays a crucial role in lowering cell-cell contacts in epithelial cells, a hallmark feature of tumor progression. Recently, Hakai was also found to interact with PSF (PTB-associated splicing factor). While PSF can function as a DNA-binding protein with a tumor suppressive function, its association with Hakai promotes PSF's RNA-binding ability and post-transcriptional influence on target mRNAs. Hakai overexpression enhanced the binding of PSF to mRNAs encoding cancer-related proteins, while knockdown of Hakai reduced the RNA-binding ability of PSF. Furthermore, the knockdown of PSF suppressed Hakai-induced cell proliferation. Thus, Hakai can affect the oncogenic phenotype both by altering E-cadherin-based intercellular adhesions and by increasing PSF's ability to bind RNAs that promote cancer-related gene expression.
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