FHL1C induces apoptosis in Notch1-dependent T-ALL cells through an interaction with RBP-J.

ABSTRACT:

Background

Aberrantly activated Notch signaling has been found in more than 50% of patients with T-cell acute lymphoblastic leukemia (T-ALL). Current strategies that employ γ-secretase inhibitors (GSIs) to target Notch activation have not been successful. Many limitations, such as non-Notch specificity, dose-limiting gastrointestinal toxicity and GSI resistance, have prompted an urgent need for more effective Notch signaling inhibitors for T-ALL treatment. Human four-and-a-half LIM domain protein 1C (FHL1C) (KyoT2 in mice) has been demonstrated to suppress Notch activation in vitro, suggesting that FHL1C may be new candidate target in T-ALL therapy. However, the role of FHL1C in T-ALL cells remained unclear.

Methods

Using RT-PCR, we amplified full-length human FHL1C, and con

SUBMITTER: Fu W 

PROVIDER: S-EPMC4077834 | biostudies-literature | 2014 Jun

REPOSITORIES: biostudies-literature