Knockdown of NAT12/NAA30 reduces tumorigenic features of glioblastoma-initiating cells.

ABSTRACT:

Background

Glioblastoma (GBM) is the most common primary brain malignancy and confers a dismal prognosis. GBMs harbor glioblastoma-initiating cells (GICs) that drive tumorigenesis and contribute to therapeutic resistance and tumor recurrence. Consequently, there is a strong rationale to target this cell population in order to develop new molecular therapies against GBM. Accumulating evidence indicates that Nα-terminal acetyltransferases (NATs), that are dysregulated in numerous human cancers, can serve as therapeutic targets.

Methods

Microarrays were used to study the expression of several NATs including NAT12/NAA30 in clinical samples and stem cell cultures. The expression of NAT12/NAA30 was analyzed using qPCR, immunolabeling and western blot. We conducted shRNA-mediated k

SUBMITTER: Mughal AA 

PROVIDER: S-EPMC4546247 | biostudies-literature | 2015 Aug

REPOSITORIES: biostudies-literature