J 2019

Sodium/calcium exchanger is involved in apoptosis induced by H2S in tumor cells through decreased levels of intracellular pH

SZADVÁRI, Ivan; Soňa HUDECOVÁ; Barbora CHOVANCOVÁ; Miroslava MATÚŠKOVÁ; Dana CHOLUJOVÁ et. al.

Basic information

Original name

Sodium/calcium exchanger is involved in apoptosis induced by H2S in tumor cells through decreased levels of intracellular pH

Authors

SZADVÁRI, Ivan; Soňa HUDECOVÁ; Barbora CHOVANCOVÁ; Miroslava MATÚŠKOVÁ; Dana CHOLUJOVÁ; Ľubomíra LENČEŠOVA; David VALERIÁN; Karol ONDRIAS; Petr BABULA and Oľga KRIŽANOVÁ

Edition

NITRIC OXIDE-BIOLOGY AND CHEMISTRY, SAN DIEGO, ACADEMIC PRESS INC ELSEVIER SCIENCE, 2019, 1089-8603

Other information

Language

English

Type of outcome

Article in a journal

Field of Study

10601 Cell biology

Country of publisher

United States of America

Confidentiality degree

is not subject to a state or trade secret

References:

Impact factor

Impact factor: 3.311

RIV identification code

RIV/00216224:14110/19:00111015

Organization unit

Faculty of Medicine

UT WoS

000466832100001

EID Scopus

2-s2.0-85062464189

Keywords in English

Apoptosis; Hydrogen sulfide; Intracellular acidification; Sodium/calcium exchanger; Sodium/hydrogen exchanger

Tags

Tags

International impact, Reviewed
Changed: 14/4/2020 14:37, Mgr. Tereza Miškechová

Abstract

In the original language

We explored possibility that sodium/calcium exchanger 1 (NCX1) is involved in pH modulation and apoptosis induction in GYY4137 treated cells. We have shown that although 10 days treatment with GYY4137 did not significantly decreased volume of tumors induced by colorectal cancer DLD1 cells in nude mice, it already induced apoptosis in these tumors. Treatment of DLD1 and ovarian cancer A2780 cells with GYY4137 resulted in intracellular acidification in a concentration-dependent manner. We observed increased mRNA and protein expression of both, NCX1 and sodium/hydrogen exchanger 1 (NHE1) in DLD1-induced tumors from GYY4137-treated mice. NCX1 was coupled with NHE1 in A2780 and DLD1 cells and this complex partially disintegrated after GYY4137 treatment. We proposed that intracellular acidification is due to uncoupling of NCX1/NHE1 complex rather than blocking of the reverse mode of NCX1, probably due to internalization of NHE1. Results might contribute to understanding molecular mechanism of H2S induced apoptosis in tumor cells.

Links

MUNI/A/1255/2018, interní kód MU
Name: Kardiovaskulární systém a jeho regulace a dysregulace pod vlivem farmak (Acronym: KAREDYSFAR)
Investor: Masaryk University, Category A