Posttranscriptional regulation of cancer gene expression programs plays a vital 
role in carcinogenesis; identifying the critical regulators of tumorigenesis and 
their molecular targets may provide novel strategies for cancer diagnosis and 
therapeutics. Highly conserved RNA-binding protein Pumilio-1 (PUM1) regulates 
mouse growth and cell proliferation, propelling us to examine its role in 
cancer. We found human PUM1 is highly expressed in a diverse group of cancer, 
including prostate cancer; enhanced PUM1 expression is also correlated with 
reduced survival among prostate cancer patients. Detailed expression analysis in 
twenty prostate cancer tissues showed enhanced expression of PUM1 at mRNA and 
protein levels. Knockdown of PUM1 reduced prostate cancer cell proliferation and 
colony formation, and subcutaneous injection of PUM1 knockdown cells led to 
reduced tumor size. Downregulation of PUM1 in prostate cancer cells consistently 
elevated cyclin-dependent kinase inhibitor 1B (CDKN1B) protein expression 
through increased translation but did not impact its mRNA level, while 
overexpression of PUM1 reduced CDKN1B protein level. Our finding established a 
critical role of PUM1 mediated translational control, particularly the 
PUM1-CDKN1B axis, in prostate cancer cell growth and tumorigenesis. We proposed 
that PUM1-CDKN1B regulatory axis may represent a novel mechanism for the loss of 
CDKN1B protein expression in diverse cancers and potential targets for 
therapeutics development.