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T-LAK 细胞起源的蛋白激酶对于肝癌 SMMC-7721 细胞的增殖是必需的。

T-LAK cell-originated protein kinase is essential for the proliferation of hepatocellular carcinoma SMMC-7721 cells.

机构信息

State Key Laboratory of Genetic Engineering, Institute of Genetics, School of Life Science, Fudan University, Shanghai, 200433, China.

出版信息

Cell Biochem Funct. 2013 Dec;31(8):736-42. doi: 10.1002/cbf.2964. Epub 2013 Mar 22.

DOI:10.1002/cbf.2964
PMID:23526201
Abstract

Hepatocellular carcinoma (HCC) is one of the most common malignancies worldwide and typically has poor prognosis. Like most cancers, altered gene expression was always associated with the induction and maintenance of HCC. Here, we reported that the expression level of T-LAK cell-originated protein kinase (TOPK) is significantly up-regulated in human HCC samples and cell lines. The suppression of TOPK by short hairpin RNA in HCC cell line SMMC-7721 caused cell cycle arrest and reduced cell growth and colony formation ability. Moreover, the tumor formation ability of the TOPK-suppression cells was significantly impaired compared with the control cells in nude mice. In addition, the knockdown expression of TOPK reduced the AKT phosphorylation. Taken together, we unveiled a novel role of TOPK which acts as an important positive regulator in human HCC cell proliferation.

摘要

肝细胞癌 (HCC) 是全球最常见的恶性肿瘤之一,通常预后不良。与大多数癌症一样,基因表达的改变与 HCC 的诱导和维持有关。在这里,我们报道 T-LAK 细胞起源蛋白激酶 (TOPK) 的表达水平在人 HCC 样本和细胞系中显著上调。在 HCC 细胞系 SMMC-7721 中,短发夹 RNA 对 TOPK 的抑制导致细胞周期停滞,并降低细胞生长和集落形成能力。此外,与对照细胞相比,TOPK 抑制细胞在裸鼠中的肿瘤形成能力显著受损。此外,TOPK 的敲低表达降低了 AKT 的磷酸化。总之,我们揭示了 TOPK 的一个新作用,它作为一个重要的正调节剂在人 HCC 细胞增殖中发挥作用。

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