Open AccessMSP58 Knockdown Inhibits the Proliferation of Esophageal Squamous Cell Carcinoma in Vitro and in Vivo
Author(s) -
Chunsheng Xu,
Jun Zheng,
Hailong Zhang,
Huadong Zhao,
Jing Zhang,
Guoqiang Wu,
Lin Wu,
Qing Wang,
Weizhong Wang,
Jian Zhang
Publication year - 2012
Publication title -
asian pacific journal of cancer prevention
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.512
H-Index - 75
eISSN - 2476-762X
pISSN - 1513-7368
DOI - 10.7314/apjcp.2012.13.7.3233
Subject(s) - cancer research , gene knockdown , oncogene , small hairpin rna , cell growth , cyclin d1 , cell cycle , biology , flow cytometry , cell , cell culture , immunology , genetics
Esophageal carcinoma (EC) is one of the most aggressive cancers with a poor prognosis. Understanding the molecular mechanisms underlying esophageal cancer progression is a high priority for improved EC diagnosis and prognosis. Recently, MSP58 was shown to behave as an oncogene in colorectal carcinomas and gliomas. However, little is known about its function in esophageal carcinomas. We therefore examined the effects of MSP58 knockdown on the growth of esophageal squamous cell carcinoma (ESCC) cells in vitro and in vivo in order to gain a better understanding of its potential as a tumor therapeutic target. We employed lentiviral-mediated small hairpin RNA (shRNA) to knock down the expression of MSP58 in the ESCC cell lines Eca-109 and EC9706 and demonstrated inhibition of ESCC cell proliferation and colony formation in vitro. Furthermore, flow cytometry and western blot analyses revealed that MSP58 depletion induced cell cycle arrest by regulating the expression of P21, CDK4 and cyclin D1. Notably, the downregulation of MSP58 significantly inhibited the growth of ESCC xenografts in nude mice. Our results suggest that MSP58 may play an important role in ESCC progression.