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Prp19 Arrests Cell Cycle via Cdc5L in Hepatocellular Carcinoma Cells
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...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5412362/ https://www.ncbi.nlm.nih.gov/pubmed/28387715 http://dx.doi.org/10.3390/ijms18040778 |
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author | Huang, Renzheng Xue, Ruyi Qu, Di Yin, Jie Shen, Xi-Zhong |
author_facet | Huang, Renzheng Xue, Ruyi Qu, Di Yin, Jie Shen, Xi-Zhong |
author_sort | Huang, Renzheng |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-5412362 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-54123622017-05-05 Prp19 Arrests Cell Cycle via Cdc5L in Hepatocellular Carcinoma Cells Huang, Renzheng Xue, Ruyi Qu, Di Yin, Jie Shen, Xi-Zhong Int J Mol Sci Article 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. MDPI 2017-04-07 /pmc/articles/PMC5412362/ /pubmed/28387715 http://dx.doi.org/10.3390/ijms18040778 Text en © 2017 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Huang, Renzheng Xue, Ruyi Qu, Di Yin, Jie Shen, Xi-Zhong Prp19 Arrests Cell Cycle via Cdc5L in Hepatocellular Carcinoma Cells |
title | Prp19 Arrests Cell Cycle via Cdc5L in Hepatocellular Carcinoma Cells |
title_full | Prp19 Arrests Cell Cycle via Cdc5L in Hepatocellular Carcinoma Cells |
title_fullStr | Prp19 Arrests Cell Cycle via Cdc5L in Hepatocellular Carcinoma Cells |
title_full_unstemmed | Prp19 Arrests Cell Cycle via Cdc5L in Hepatocellular Carcinoma Cells |
title_short | Prp19 Arrests Cell Cycle via Cdc5L in Hepatocellular Carcinoma Cells |
title_sort | prp19 arrests cell cycle via cdc5l in hepatocellular carcinoma cells |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5412362/ https://www.ncbi.nlm.nih.gov/pubmed/28387715 http://dx.doi.org/10.3390/ijms18040778 |
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