Open AccessSilencing P12CDK2AP1 with a lentivirus promotes HaCaT cell proliferation
Author(s) -
Miao Sun,
Jiawei Zheng,
Hui Xue,
Yuguang Jiang,
Chunnan Li,
LI Jian-hu,
Wei Jin,
Minzhi Shen,
Xiangming Yang,
Qianwei Ni
Publication year - 2012
Publication title -
molecular medicine reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.727
H-Index - 56
eISSN - 1791-3004
pISSN - 1791-2997
DOI - 10.3892/mmr.2012.1205
Subject(s) - hacat , rna interference , small interfering rna , small hairpin rna , gene knockdown , gene silencing , biology , cell cycle , lentivirus , microbiology and biotechnology , cell growth , oncogene , cancer research , cell , cell culture , transfection , rna , gene , virology , genetics , virus , viral disease
The tumor suppressor P12CDK2AP1 negatively regulates cyclin-dependent kinase 2 (CDK2) activities and suppresses DNA replication. Notably, P12CDK2AP1 is known to be downregulated in head and neck squamous cell carcinomas (HNSCCs). Silencing of specific gene expression by small interfering RNAs (siRNAs) or short hairpin RNAs (shRNAs) using expression vectors and retroviruses has become a powerful tool for the genetic analysis of mammalian cells. In the present study, we utilized lentivirus‑mediated shRNA for functional gene knockdown in normal human skin keratinocytes (HaCaT) cells in order to assess the potential role of P12CDK2AP1 in HNSCCs. Lentivirus‑mediated RNA interference (RNAi) effectively reduced endogenous P12CDK2AP1 expression in HaCaT cells and significantly promoted HaCaT cell proliferation in vitro. Lentiviral vectors have the ability to infect dividing and non-dividing cells as well as to achieve long‑term multilineage gene expression. Thus, additional studies are needed to investigate the use of such vectors as a therapeutic tool for the delivery of siRNAs.