Další formáty:
BibTeX
LaTeX
RIS
@article{2415997,
author = {Nalla, Lakshmi Vineela and Khairnar, Amit Suresh},
article_location = {NEW YORK},
article_number = {August 2024},
doi = {http://dx.doi.org/10.1016/j.freeradbiomed.2024.05.018},
keywords = {Ferroptosis; Reactive oxygen species; Breast cancer; Metastasis; Anoikis resistance},
language = {eng},
issn = {0891-5849},
journal = {Free Radical Biology and Medicine},
title = {Empagliflozin drives ferroptosis in anoikis-resistant cells by activating miR-128-3p dependent pathway and inhibiting CD98hc in breast cancer},
url = {https://www.sciencedirect.com/science/article/pii/S0891584924004532?via%3Dihub},
volume = {220},
year = {2024}
}
TY - JOUR
ID - 2415997
AU - Nalla, Lakshmi Vineela - Khairnar, Amit Suresh
PY - 2024
TI - Empagliflozin drives ferroptosis in anoikis-resistant cells by activating miR-128-3p dependent pathway and inhibiting CD98hc in breast cancer
JF - Free Radical Biology and Medicine
VL - 220
IS - August 2024
SP - 288-300
EP - 288-300
PB - ELSEVIER SCIENCE INC
SN - 08915849
KW - Ferroptosis
KW - Reactive oxygen species
KW - Breast cancer
KW - Metastasis
KW - Anoikis resistance
UR - https://www.sciencedirect.com/science/article/pii/S0891584924004532?via%3Dihub
N2 - A tumour suppressor miRNA, miR-128-3p, is widely involved in various biological processes and has been found to get downregulated in breast cancer patients. We previously published that ectopically expressed miR-128-3p suppressed migration, invasion, cell cycle arrest, and breast cancer stem cells. In the present study, we explored the role of Empagliflozin (EMPA) as a miR-128-3p functionality-mimicking drug in inducing ferroptosis by inhibiting CD98hc. Given that CD98hc is one of the proteins critical in triggering ferroptosis, we confirmed that miR-128-3p and EMPA inhibited SP1, leading to inhibition of CD98hc expression. Further, transfection with siCD98hc, miR-128-3p mimics, and inhibitors was performed to assess their involvement in the ferroptosis of anoikis-resistant cells. We proved that anoikis-resistant cells possess high ROS and iron levels. Further, miR-1283p and EMPA treatments induced ferroptosis by inhibiting GSH and enzymatic activity of GPX4 and also induced lipid peroxidation. Moreover, EMPA suppressed bioluminescence of 4T1-Red-FLuc induced thoracic cavity, peritoneal tumour burden and lung nodules in an in-vivo metastatic model of breast cancer. Collectively, we revealed that EMPA sensitized the ECM detached cells to ferroptosis by synergically activating miR-128-3p and lowering the levels of SP1 and CD98hc, making it a potential adjunct drug for breast cancer chemotherapy.
ER -
NALLA, Lakshmi Vineela a Amit Suresh KHAIRNAR. Empagliflozin drives ferroptosis in anoikis-resistant cells by activating miR-128-3p dependent pathway and inhibiting CD98hc in breast cancer. \textit{Free Radical Biology and Medicine}. NEW YORK: ELSEVIER SCIENCE INC, 2024, roč.~220, August 2024, s.~288-300. ISSN~0891-5849. Dostupné z: https://dx.doi.org/10.1016/j.freeradbiomed.2024.05.018.
|
