克服头颈部鳞状细胞癌中西妥昔单抗的耐药性：AURKB 和 DUSP 蛋白的作用。
Overcoming cetuximab resistance in HNSCC: the role of AURKB and DUSP proteins.
机构信息
Center for Oncological Research (CORE) Antwerp, Laboratory of Cancer Research and Clinical Oncology, University of Antwerp, Universiteitsplein1, Wilrijk, Belgium.
Center for Oncological Research (CORE) Antwerp, Laboratory of Cancer Research and Clinical Oncology, University of Antwerp, Universiteitsplein1, Wilrijk, Belgium; Center for Medical Genetics, Department of Biomedical Sciences, University of Antwerp, Universiteitsplein1, Wilrijk, Belgium; Antwerp University Hospital, Wilrijkstraat 10, Antwerpen, Belgium.
出版信息
Cancer Lett. 2014 Nov 28;354(2):365-77. doi: 10.1016/j.canlet.2014.08.039. Epub 2014 Sep 2.
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.
阐明头颈部鳞状细胞癌（HNSCC）中西妥昔单抗耐药的潜在机制非常重要，因为许多肿瘤仍然没有反应或产生耐药性。我们的微阵列结果表明，“耐药”细胞仍然表现出 RAS-MAPK 通路信号，这有助于产生耐药性，这表现在 ERK1/2 的负调控因子 DUSP5 和 DUSP6 的低表达，以及有丝分裂关键调节因子 AURKB 的高表达。因此，通过 ERK1/2 抑制剂（芹菜素）或 AURKB 抑制剂（巴拉斯替尼）阻断 RAS-MAPK 通路可能是克服 HNSCC 中西妥昔单抗耐药的一种新策略。
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