@Article{biocell.2024.050701,
AUTHOR = {YU-YAN LAN, TSUN-CHIH CHENG, YI-PING LEE, CHIA-YIH WANG, BU-MIIN HUANG},
TITLE = {Paclitaxel induces human KOSC3 oral cancer cell apoptosis through caspase pathways},
JOURNAL = {BIOCELL},
VOLUME = {48},
YEAR = {2024},
NUMBER = {7},
PAGES = {1047--1054},
URL = {http://www.techscience.com/biocell/v48n7/57225},
ISSN = {1667-5746},
ABSTRACT = { <b>Background:</b> Paclitaxel is a compound derived from Pacific yew bark that induces various cancer cell apoptosis. However, whether it also has anticancer activities in KOSC3 cells, an oral cancer cell line, is unclear. <b>Methods:</b> 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, flow cytometry, and western blotting assays were carried out to assess cell viability, subG1 phase of the cell cycle, and apoptosis-related protein expression, respectively. <b>Results:</b> Our findings indicate that paclitaxel could inhibit cell viability and increase the expression of apoptotic markers, including plasma membrane blebbing and the cleavage of poly ADP-ribose polymerase in KOSC3 cells. Also, the treatment with paclitaxel remarkably elevated the percentage of the subG1 phase in KOSC3 cells. In addition, treatment with a pan-caspase inhibitor could recover paclitaxel-inhibited cell viability. Moreover, caspase-8, caspase-9, caspase-7, and BH3 interacting domain death agonist (Bid) were activated in paclitaxel-treated KOSC3 cells. <b>Conclusions:</b> Paclitaxel induced apoptosis through caspase cascade in KOSC3 cells.},
DOI = {10.32604/biocell.2024.050701}
}