当前位置： SCI文献检索 > BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS期刊下所有文献 > GDC-0980 (apitolisib) treatment with gemcitabine and/or cisplatin synergistically reduces cholangiocarcinoma cell growth by suppressing the PI3K/Akt/mTOR pathway.

GDC-0980 (apitolisib) treatment with gemcitabine and/or cisplatin synergistically reduces cholangiocarcinoma cell growth by suppressing the PI3K/Akt/mTOR pathway.

Abstract：

:Since conventional chemotherapy (gemcitabine and cisplatin) has marginal survival benefit in patients with advanced cholangiocarcinoma (CCA), an effective targeted therapeutic agent is urgently required. Activation of the PI3K/Akt/mTOR signaling pathway is frequently observed in CCA, and thus, PI3K and mTOR are promising therapeutic targets in CCA. Recently a new dual PI3K/mTOR inhibitor GDC-0980 (apitolisib) was introduced. This study was undertaken to examine the activity of apitolisib against CCA cells in vitro and in vivo. Apitolisib treatment strongly reduced Akt and mTOR active phosphorylation levels and attenuated cell growth in two different CCA cell lines (SNU478 and SNU1196). In addition, the cytotoxic activity of apitolisib enhanced the effects of gemcitabine or cisplatin in vitro and increased PARP cleavage. Moreover, we observed these co-treatments significantly reduced colony formation by SNU478 and SNU1196 cells and potently inhibited tumor growth in a mouse xenograft model. The results of the present study show that apitolisib effectively reduces CCA cell growth by suppressing the PI3K/Akt/mTOR pathway. In addition, co-treatments with apitolisib and gemcitabine or cisplatin synergistically enhanced apitolisib activity, which suggests a means of improving the chemotherapeutic sensitivity of CCA.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Jang DK,Lee YG,Chan Chae Y,Lee JK,Paik WH,Lee SH,Kim YT,Ryu JK

doi

10.1016/j.bbrc.2020.06.011

subject

Has Abstract

pub_date

2020-09-03 00:00:00

pages

1242-1248

issue

4

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(20)31205-5

journal_volume

529

pub_type

杂志文章

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