Prp19 Arrests Cell Cycle via Cdc5L in Hepatocellular Carcinoma Cells.
Prp19 Arrests Cell Cycle via Cdc5L in Hepatocellular Carcinoma Cells.
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Prp19 通过 Cdc5L 阻止肝细胞癌细胞的细胞周期
DOI：
10.3390/ijms18040778
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发表时间：
2017-04-07
影响因子：
5.6
通讯作者：
Shen XZ
中科院分区：
文献类型：
--
作者：
Huang R;Xue R;Qu D;Yin J;Shen XZ
前体mRNA加工因子19（Prp 19）参与许多细胞事件，包括前体mRNA加工和DNA损伤反应。最近，它已被确定为肝细胞癌（HCC）的候选癌基因。然而，Prp 19在肿瘤生物学中的作用仍然难以捉摸。我们报道了Prp 19通过调控G2/M期转换阻滞肝癌细胞的细胞周期。机制的见解表明，沉默Prp 19抑制细胞分裂周期5样（Cdc 5L）的表达，通过抑制Cdc 5L mRNA的翻译和促进溶酶体介导的降解Cdc 5L在肝癌细胞。此外，我们发现，沉默Prp 19诱导的细胞周期停滞可以部分恢复过表达Cdc 5L。这项工作意味着Prp 19参与有丝分裂进程，因此可能是一个有前途的治疗肝癌的目标。
Pre-mRNA processing factor 19 (Prp19) is involved in many cellular events including pre-mRNA processing and DNA damage response. Recently, it has been identified as a candidate oncogene in hepatocellular carcinoma (HCC). However, the role of Prp19 in tumor biology is still elusive. Here, we reported that Prp19 arrested cell cycle in HCC cells via regulating G2/M transition. Mechanistic insights revealed that silencing Prp19 inhibited the expression of cell division cycle 5-like (Cdc5L) via repressing the translation of Cdc5L mRNA and facilitating lysosome-mediated degradation of Cdc5L in HCC cells. Furthermore, we found that silencing Prp19 induced cell cycle arrest could be partially resumed by overexpressing Cdc5L. This work implied that Prp19 participated in mitotic progression and thus could be a promising therapeutic target of HCC.