MSP58 Knockdown Inhibits the Proliferation of EsophagealSquamous Cell Carcinoma in Vitro and in Vivo

Esophageal carcinoma (EC) is one of the most aggressive cancers with a poor prognosis. Understanding themolecular mechanisms underlying esophageal cancer progression is a high priority for improved EC diagnosisand 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 MSP58knockdown on the growth of esophageal squamous cell carcinoma (ESCC) cells in vitro and in vivo in order togain a better understanding of its potential as a tumor therapeutic target. We employed lentiviral-mediated smallhairpin RNA (shRNA) to knock down the expression of MSP58 in the ESCC cell lines Eca-109 and EC9706 anddemonstrated inhibition of ESCC cell proliferation and colony formation in vitro. Furthermore, flow cytometryand western blot analyses revealed that MSP58 depletion induced cell cycle arrest by regulating the expressionof P21, CDK4 and cyclin D1. Notably, the downregulation of MSP58 significantly inhibited the growth of ESCCxenografts in nude mice. Our results suggest that MSP58 may play an important role in ESCC progression.