LISKOVA, Veronika, Barbora CHOVANCOVA, Kristina GALVANKOVA, Ladislav KLENA, Katarina MATYASOVA, Petr BABULA, Marian GRMAN, Ingeborg REZUCHOVA, Maria BARTOSOVA and Oľga KRIŽANOVÁ. Slow Sulfide Donor GYY4137 Increased the Sensitivity of Two Breast Cancer Cell Lines to Paclitaxel by Different Mechanisms. Biomolecules. Basel: MDPI, 2024, vol. 14, No 6, p. 1-17. ISSN 2218-273X. Available from: https://dx.doi.org/10.3390/biom14060651.
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Basic information
Original name Slow Sulfide Donor GYY4137 Increased the Sensitivity of Two Breast Cancer Cell Lines to Paclitaxel by Different Mechanisms
Authors LISKOVA, Veronika, Barbora CHOVANCOVA, Kristina GALVANKOVA, Ladislav KLENA, Katarina MATYASOVA, Petr BABULA (203 Czech Republic, belonging to the institution), Marian GRMAN, Ingeborg REZUCHOVA, Maria BARTOSOVA and Oľga KRIŽANOVÁ (703 Slovakia, belonging to the institution).
Edition Biomolecules, Basel, MDPI, 2024, 2218-273X.
Other information
Original language English
Type of outcome Article in a journal
Field of Study 10608 Biochemistry and molecular biology
Country of publisher Switzerland
Confidentiality degree is not subject to a state or trade secret
WWW URL
Impact factor Impact factor: 5.500 in 2022
Organization unit Faculty of Medicine
Doi http://dx.doi.org/10.3390/biom14060651
UT WoS 001254538200001
Keywords in English paclitaxel; breast cancer cell lines; apoptosis; slow sulfide donor; metabolism
Tags 14110515, rivok
Tags International impact, Reviewed
Changed by Changed by: Mgr. Tereza Miškechová, učo 341652. Changed: 9/7/2024 12:01.
Abstract
Paclitaxel (PTX) is a chemotherapeutic agent affecting microtubule polymerization. The efficacy of PTX depends on the type of tumor, and its improvement would be beneficial in patients' treatment. Therefore, we tested the effect of slow sulfide donor GYY4137 on paclitaxel sensitivity in two different breast cancer cell lines, MDA-MB-231, derived from a triple negative cell line, and JIMT1, which overexpresses HER2 and is resistant to trastuzumab. In JIMT1 and MDA-MB-231 cells, we compared IC50 and some metabolic (apoptosis induction, lactate/pyruvate conversion, production of reactive oxygen species, etc.), morphologic (changes in cytoskeleton), and functional (migration, angiogenesis) parameters for PTX and PTX/GYY4137, aiming to determine the mechanism of the sensitization of PTX. We observed improved sensitivity to paclitaxel in the presence of GYY4137 in both cell lines, but also some differences in apoptosis induction and pyruvate/lactate conversion between these cells. In MDA-MB-231 cells, GYY4137 increased apoptosis without affecting the IP3R1 protein, changing the morphology of the cytoskeleton. A mechanism of PTX sensitization by GYY4137 in JIMT1 cells is distinct from MDA-MB-231, and remains to be further elucidated. We suggest different mechanisms of action for H2S on the paclitaxel treatment of MDA-MB-231 and JIMT1 breast cancer cell lines.
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