| Literature DB >> 25192874 |
Carolien Boeckx1, Ken Op de Beeck2, An Wouters3, Vanessa Deschoolmeester3, Ridha Limame3, Karen Zwaenepoel4, Pol Specenier5, Patrick Pauwels6, Jan B Vermorken5, Marc Peeters5, Guy Van Camp7, Marc Baay3, Filip Lardon3.
Abstract
Unraveling the underlying mechanisms of cetuximab resistance in head and neck squamous cell carcinoma (HNSCC) is of major importance as many tumors remain non-responsive or become resistant. Our microarray results suggest that "resistant" cells still exhibit RAS-MAPK pathway signaling contributing to drug resistance, as witnessed by low expression of DUSP5 and DUSP6, negative regulators of ERK1/2, and increased expression of AURKB, a key regulator of mitosis. Therefore, interrupting the RAS-MAPK pathway by an ERK1/2 inhibitor (apigenin) or an AURKB inhibitor (barasertib) might be a new strategy for overcoming cetuximab resistance in HNSCC.Entities:
Keywords: Anti-EGFR therapy; Aurora kinase B; Cetuximab resistance; Dual-specificity phosphatase 5 and 6; Head and neck squamous cell carcinoma; NanoPro 1000
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Year: 2014 PMID： 25192874 DOI： 10.1016/j.canlet.2014.08.039
Source DB: PubMed Journal: Cancer Lett ISSN： 0304-3835 Impact factor: 8.679