Accumulated SET protein up-regulates and interacts with hnRNPK, increasing its binding to nucleic acids, the Bcl-xS repression, and cellular proliferation
Accumulated SET protein up-regulates and interacts with hnRNPK, increasing its binding to nucleic acids, the Bcl-xS repression, and cellular proliferation
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DOI：
10.1016/j.bbrc.2014.01.175
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发表时间：
2014-02-28
影响因子：
3.1
通讯作者：
Leopoldino, Andreia M.
中科院分区：
文献类型：
--
作者：
Almeida, Luciana O.;Garcia, Cristiana B.;Leopoldino, Andreia M.
SET和hnRNPK是参与基因表达和细胞信号传导调节的蛋白质。我们先前证明SET在头颈部鳞状细胞癌（HNSCC）中积累; hnRNPK是癌症的预后标志物。在这里，我们假设SET和hnRNPK蛋白相互作用，以促进肿瘤发生。我们分别在SET/hnRNPK过表达和敲低的HEK 293和HNSCC（HN 6、HN 12和HN 13）细胞系中进行了研究。我们发现SET和/或hnRNPK蛋白积累增加细胞增殖。SET积累上调hnRNPK mRNA和总蛋白/磷酸化蛋白，促进hnRNPK核定位，并降低Bcl-x mRNA水平。SET蛋白直接与hnRNPK相互作用，增加其与核酸的结合和Bcl-xS抑制。我们建议，hnRNPK应该是一个新的目标，SET和hnRNPK的相互作用，反过来，有潜在的影响，在细胞的生存和恶性转化。(C)2014爱思唯尔公司All rights reserved.
SET and hnRNPK are proteins involved in gene expression and regulation of cellular signaling. We previously demonstrated that SET accumulates in head and neck squamous cell carcinoma (HNSCC); hnRNPK is a prognostic marker in cancer. Here, we postulate that SET and hnRNPK proteins interact to promote tumorigenesis. We performed studies in HEK293 and HNSCC (HN6, HN12, and HN13) cell lines with SET/hnRNPK overexpression and knockdown, respectively. We found that SET and/or hnRNPK protein accumulation increased cellular proliferation. SET accumulation up-regulated hnRNPK mRNA and total/phosphorylated protein, promoted hnRNPK nuclear location, and reduced Bcl-x mRNA levels. SET protein directly interacted with hnRNPK, increasing both its binding to nucleic acids and Bcl-xS repression. We propose that hnRNPK should be a new target of SET and that SET-hnRNPK interaction, in turn, has potential implications in cell survival and malignant transformation. (C) 2014 Elsevier Inc. All rights reserved.