PRP19 upregulation inhibits cell proliferation in lung adenocarcinomas by p21-mediated induction of cell cycle arrest

Arko Boham Benjamin, Xin Zhou, Okai Isaac, Haoqi Zhao, Yang Song, Xinming Chi, Bing Sun, Lihong Hao, Liyuan Zhang, Lu Liu, Hongwei Guan, Shujuan Shao

Research output: Contribution to journalArticlepeer-review

11 Citations (Scopus)

Abstract

Precursor messenger RNA processing factor 19 (PRP19) is known to be a critical component of the eukaryotic spliceosomal machinery and DNA damage repair system, the deregulation of which leads to many disease conditions. In many human cancers, PRP19 expression is upregulated, but its functional significance and corresponding underlying mechanisms remain to be addressed. Focusing on lung carcinomas, PRP19 upregulation was achieved by plasmid transfection into A549 adenocarcinoma cells. The transfected cells were then subjected to several in vitro and in vivo assays following in situ assessment of the protein in paired clinical lung tissues. We report that PRP19 expression is elevated in lung carcinoma tissues compared to non-tumor tissues. Following its upregulation, PRP19 repressed cell proliferation and tumor growth by upregulating the expression of the cell cycle arrest protein p21.

Original languageEnglish
Pages (from-to)463-470
Number of pages8
JournalBiomedicine and Pharmacotherapy
Volume68
Issue number4
DOIs
Publication statusPublished - May 2014

Keywords

  • Cell proliferation
  • Lung carcinoma
  • P21
  • PRP19

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