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Mitochondrial NOS1 suppresses apoptosis in colon cancer cells through increasing SIRT3 activity.

Abstract：

:Previous studies have suggested that nitric oxide (NO) which is synthetized by nitric oxide synthase (NOS) is closely related to the carcinogenesis and progression of colon cancer. However, the precise physiopathological role of NO on colon cancer remains unclear, and a lot of related studies focused on NOS2 and NOS3, but little on NOS1. Here, stable overexpression NOS1 of colon cancer cells were constructed to investigate whether NOS1 plays a special role in colon cancer. We observed that NOS1 protein was presented in mitochondria. Both the basal and cisplatin-induced mitochondrial superoxide were inhibited by NOS1, and the cisplatin-induced apoptosis was also inhibited by NOS1. Geldanamycin, a Hsp90 N-terminal inhibitor, was able to impede NOS1 translocation into mitochondria and reverse NOS1-induced apoptosis resistance. Importantly, SIRT3 activity was enhanced by NOS1, which contributes to the low level of mitochondrial superoxide and apoptosis resistance. Our data suggest a link between NOS1 and apoptosis resistance in colon cancer cells through mtNOS1-SIRT3-SOD2 axis. Furthermore, NOS1-induced apoptosis resistance could be reversed by inhibiting mitochondrial translocation of NOS1.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Wang Q,Ye S,Chen X,Xu P,Li K,Zeng S,Huang M,Gao W,Chen J,Zhang Q,Zhong Z,Liu Q

doi

10.1016/j.bbrc.2019.05.114

subject

Has Abstract

pub_date

2019-08-06 00:00:00

pages

517-523

issue

4

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(19)31000-9

journal_volume

515

pub_type

杂志文章

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