QKI-5 suppresses cyclin D1 expression and proliferation of oral squamous cell carcinoma cells via MAPK signalling pathway
QKI-5 suppresses cyclin D1 expression and proliferation of oral squamous cell carcinoma cells via MAPK signalling pathway
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DOI：
10.1016/j.ijom.2014.10.001
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发表时间：
2015-05-01
影响因子：
2.4
通讯作者：
Feng, Y.
中科院分区：
文献类型：
--
作者：
Fu, X.;Feng, Y.
口腔鳞状细胞癌（Oral squamous cell carcinoma，OSCC）是世界上最常见的恶性肿瘤之一。RNA结合蛋白震颤（QKI）是一种新发现的肿瘤抑制因子，在多种癌症中，但其在口腔鳞癌中的作用目前尚不清楚。本研究的目的是阐明QKI表达与OSCC发展之间的关系。我们发现QKI-5在口腔癌细胞系CAL-27中的表达显著降低。QKI-5过表达也降低CAL-27细胞的增殖，这与cyclin D1相关。QKI-5的这种调节功能通过调节促分裂原活化蛋白激酶（MAPK）途径的磷酸化水平而发生。因此，本研究表明，肿瘤抑制因子QKI-5的低表达可以激活MAPK通路，并有助于不受控制的细胞周期蛋白D1的表达，从而导致口腔癌细胞增殖增加。
Oral squamous cell carcinoma (OSCC) is one of the most frequently occurring malignancies in the world. The RNA-binding protein quaking (QKI) is a newly identified tumour suppressor in multiple cancers, but its role in OSCC is currently unknown. The purpose of the present study was to clarify the relationship between QKI expression and OSCC development. We found QKI-5 expression to be significantly decreased in the oral cancer cell line CAL-27. QKI-5 overexpression also reduced the proliferation of CAL-27 cells, which correlated with cyclin D1. This regulative function of QKI-5 occurs by modulating the phosphorylation level of the mitogen-activated protein kinase (MAPK) pathway. Therefore this study shows that underexpression of tumour suppressor QKI-5 could activate the MAPK pathway and contribute to uncontrolled cyclin D1 expression, thus resulting in increased proliferation of oral cancer cells.