Accurate gene expression requires the precise control of mRNA levels, which are 
determined by the relative rates of nuclear (pre-)mRNA synthesis and processing, 
and cytoplasmic mRNA turnover. A key step in mRNA degradation is the removal of 
the poly(A) tail, which involves several deadenylases including components of 
the Ccr4-Not complex. Here, we focused on the role of the human paralogues CNOT7 
(hCaf1/Caf1a) and CNOT8 (hPop2/Caf1b/Calif), which possess deadenylase activity 
mediated by DEDD nuclease domains. We show that efficient proliferation requires 
both subunits, although combined knockdown of CNOT7 and CNOT8 further reduces 
cell proliferation indicating partial redundancy between these proteins. 
Interestingly, the function of CNOT7 in cell proliferation partly depends on its 
catalytic activity. On the other hand, the interaction between CNOT7 and BTG2, a 
member of the antiproliferative BTG/Tob family involved in transcription and 
mRNA decay appears less important for proliferation of MCF7 cells, suggesting 
that CNOT7 does not function solely in conjunction with BTG2. Further analysis 
of gene expression profiles of CNOT7 and/or CNOT8 knockdown cells underscores 
the partial redundancy between these subunits and suggests that regulation of 
several genes, including repression of the antiproliferative genes MSMB and 
PMP22, by the Ccr4-Not complex contributes to cell proliferation.