Abstract:
:Enhanced Notch signaling contributes to uncontrolled cell growth and cell death resistance in cancer. Here, we demonstrate that in colorectal carcinoma cells the Notch1-dependent activation of cell cycle and proliferation is mediated by repression of the cyclin-dependent kinase inhibitor (CDKI) p27. The half-life of p27 significantly increased after siRNA‑mediated knockdown of Notch1. Notch1 depletion altered the transcription of SKP2, KPC1 and KPC2, which are E3-ubiquitin ligase subunits targeting p27 for proteasomal degradation in the nucleus and the cytoplasm, respectively. As a consequence, the levels of p27 in both cellular fractions were elevated upon Notch1 knockdown. Importantly, the downregulation of Notch1 significantly sensitized colorectal cancer cells to chemotherapy and ionizing radiation. Our findings support an important role of p27 in Notch1-dependent oncogenic signaling and suggest that Notch1 is a promising target for an experimental therapy of colorectal carcinoma.
journal_name
Int J Oncoljournal_title
International journal of oncologyauthors
Hristova NR,Tagscherer KE,Fassl A,Kopitz J,Roth Wdoi
10.3892/ijo.2013.2140subject
Has Abstractpub_date
2013-12-01 00:00:00pages
1967-75issue
6eissn
1019-6439issn
1791-2423journal_volume
43pub_type
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