The impact of S6K1 kinase on neuroblastoma cell proliferation is independent of GLI1 signaling.

ABSTRACT:

Background

The crosstalk between Hedgehog (HH) signaling and other signal transduction cascades has been extensively studied in different cancers. In neuroblastoma, mTOR/S6K1 signaling is known to have a role in the development of this disease and recent evidence also implicates the HH pathway. Moreover, S6K1 kinase has been shown to phosphorylate GLI1, the effector of HH signaling, promoting GLI1 transcriptional activity and oncogenic function in esophageal adenocarcinoma. In this study, we examined the possible interplay of S6K1 and GLI1 signaling in neuroblastoma.

Methods

siRNA knockdowns were used to suppress S6K1 and GLI1 expression, and the siRNA effects were validated by real-time PCR and Western blotting. Cell proliferation analysis was performed with the EdU incorpo

SUBMITTER: Diao Y 

PROVIDER: S-EPMC4152578 | biostudies-literature | 2014 Aug

REPOSITORIES: biostudies-literature