C20orf27 Promotes Cell Growth and Proliferation of Colorectal Cancer via the TGFβR-TAK1-NFĸB Pathway.

Background: 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. Methods and Results: In this study, by using WST-1 (Highly water-soluble tetrazolium salt-1) and colony formation assays, we found that C20orf27 (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 C20orf27 promoted the growth of CRC. Signal pathway analysis identified the TGF beta R-TAK1-NFkB cascade as a mediator in C20orf27-induced CRC progression. Inhibition experiments using NFkB inhibitors reversed this progression. Co-immunoprecipitation showed that C20orf27 promoted the activation of the TGF beta R-TAK1-NFkB pathway by interacting with PP1c (the catalytic subunit of type 1 phosphatase). Conclusions: Our results firstly characterized the functional role and molecular mechanism of C20orf27 in driving CRC growth and proliferation through the TGF beta R-TAK1-NFkB pathway, suggesting its potential as a novel CRC candidate therapeutic target and tumor marker.