: 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. : In this study, by using WST-1 (Highly water-soluble tetrazolium salt-1) and colony formation assays, we found that (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 promoted the growth of CRC. Signal pathway analysis identified the TGFβR-TAK1-NFĸB cascade as a mediator in -induced CRC progression. Inhibition experiments using NFĸB inhibitors reversed this progression. Co-immunoprecipitation showed that promoted the activation of the TGFβR-TAK1-NFĸB pathway by interacting with PP1c (the catalytic subunit of type 1 phosphatase). : Our results firstly characterized the functional role and molecular mechanism of 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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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7072304 | PMC |
http://dx.doi.org/10.3390/cancers12020336 | DOI Listing |
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