Summary: | <i>Background</i>: Colorectal cancer (CRC) is a high incidence of malignant tumors that lacks highly effective and targeted drugs and thus it is in urgent need of finding new specific molecular targets. <i>Methods and Results</i>: In this study, by using WST-1 (Highly water-soluble tetrazolium salt-1) and colony formation assays, we found that <i>C20orf27</i> (chromosome 20 open reading frame 27), a functionally unknown protein, enhanced the growth and proliferation of CRC cells. The nude mouse tumor formation experiments verified that <i>C20orf27</i> promoted the growth of CRC. Signal pathway analysis identified the TGFβR-TAK1-NFĸB cascade as a mediator in <i>C20orf27</i>-induced CRC progression. Inhibition experiments using NFĸB inhibitors reversed this progression. Co-immunoprecipitation showed that <i>C20orf27</i> promoted the activation of the TGFβR-TAK1-NFĸB pathway by interacting with PP1c (the catalytic subunit of type 1 phosphatase). <i>Conclusions</i>: Our results firstly characterized the functional role and molecular mechanism of <i>C20orf27</i> in driving CRC growth and proliferation through the TGFβR-TAK1-NFĸB pathway, suggesting its potential as a novel CRC candidate therapeutic target and tumor marker.
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