J 2022

Slow sulfide donor GYY4137 potentiates effect of paclitaxel on colorectal carcinoma cells

KAJSIK, Marek, Barbora CHOVANCOVA, Veronika LISKOVA, Petr BABULA, Oľga KRIŽANOVÁ et. al.

Základní údaje

Originální název

Slow sulfide donor GYY4137 potentiates effect of paclitaxel on colorectal carcinoma cells

Autoři

KAJSIK, Marek, Barbora CHOVANCOVA, Veronika LISKOVA, Petr BABULA (203 Česká republika, domácí) a Oľga KRIŽANOVÁ (703 Slovensko, garant, domácí)

Vydání

European Journal of Pharmacology, AMSTERDAM, Elsevier, 2022, 0014-2999

Další údaje

Jazyk

angličtina

Typ výsledku

Článek v odborném periodiku

Obor

30105 Physiology

Stát vydavatele

Nizozemské království

Utajení

není předmětem státního či obchodního tajemství

Odkazy

Impakt faktor

Impact factor: 5.000

Kód RIV

RIV/00216224:14110/22:00128274

Organizační jednotka

Lékařská fakulta

UT WoS

000783277500001

Klíčová slova anglicky

Colorectal carcinoma cells; Paclitaxel; H2S; Slow sulfide donor GYY4137

Štítky

Příznaky

Mezinárodní význam, Recenzováno
Změněno: 25. 1. 2023 13:26, Mgr. Tereza Miškechová

Anotace

V originále

Although paclitaxel (PTX) is potent chemotherapeutic agent commonly used in variety of cancers, in colorectal carcinoma its usage is excluded because of low effectivity. Up to now, some experimental attempts were utilized to improve sensitivity of colorectal carcinoma to PTX. We used a slow sulfide donor GYY4137 to increase sensitivity of colorectal carcinoma cells to PTX. As a model of colorectal carcinoma, we utilized three different cell lines - HCT116, SW620 and DLD1. We compared IC50 for PTX and PTX/GYY4137, cell cycle, apoptosis, ATP levels and changes in intracellular pH. We observed significant decrease in IC50 levels in PTX/GYY4137 groups compared to PTX in all three cell lines. PTX arrested cell cycle in G2/M phase. Differences in S phase were observed in HCT116 and DLD1 cells treated with 20 nM PTX/GYY4137, but not in SW620 cell. GYY4137 increased early, but not late phase of apoptosis. This increase was not detected in non-cancer EAHy926 cells. Upregulation of IP3R1 suggested involvement of these receptors in PTX and/or GYY4137 induced apoptosis. We also observed partial ATP depletion and intracellular acidification in PTX treated groups. In PTX/GYY4137 groups of all three cell lines no ATP depletion was detectable and intracellular acidification was lower than in PTX treated groups. Slight differences in all measured parameters were determined among HCT116, SW620 and DLD1 cells, which is probably due to physiological variations in these cells. Taking together, sensitivity of PTX to colorectal carcinoma cell lines could be increased by slow sulfide donor GYY4137, probably through potentiation of apoptosis.