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mTOR inhibition sensitizes human hepatocellular carcinoma cells to resminostat.

Abstract：

:Histone deacetylases (HDACs) hyper-activity in hepatocellular carcinoma (HCC) is often associated with patients' poor prognosis. Our previous study has shown that resminostat, a novel HDAC inhibitor (HDACi), activated mitochondrial permeability transition pore (mPTP)-dependent apoptosis pathway in HCC cells. Here we explored the potential resminostat resistance factor by focusing on mammalian target of rapamycin (mTOR). We showed that AZD-2014, a novel mTOR kinase inhibitor, potentiated resminostat-induced cytotoxicity and proliferation inhibition in HCC cells. Molecularly, AZD-2014 enhanced resminostat-induced mPTP apoptosis pathway activation in HCC cells. Inhibition of this apoptosis pathway, by the caspase-9 specific inhibitor Ac-LEHD-CHO, the mPTP blockers (sanglifehrin A/cyclosporine A), or by shRNA-mediated knockdown of mPTP component cyclophilin-D (Cyp-D), significantly attenuated resminostat plus AZD-2014-induced cytotoxicity and apoptosis in HCC cells. Significantly, mTOR shRNA knockdown or kinase-dead mutation (Asp-2338-Ala) also sensitized HCC cells to resminostat, causing profound cytotoxicity and apoptosis induction. Together, these results suggest that mTOR could be a primary resistance factor of resminostat. Targeted inhibition of mTOR may thus significantly sensitize HCC cells to resminostat.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Peng X,Zhang D,Li Z,Fu M,Liu H

doi

10.1016/j.bbrc.2016.06.060

subject

Has Abstract

pub_date

2016-09-02 00:00:00

pages

556-562

issue

4

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(16)30978-0

journal_volume

477

pub_type

杂志文章

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