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Home / Journals / BIOCELL / Online First / doi:10.32604/biocell.2024.050701
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ARTICLE

Paclitaxel induces human KOSC3 oral cancer cell apoptosis through caspase pathways

YU-YAN LAN1,#, TSUN-CHIH CHENG2,#, YI-PING LEE3, CHIA-YIH WANG3,*, BU-MIIN HUANG3,4,*
1 School of Medicine, College of Medicine, I-Shou University, Kaohsiung, 82445, Taiwan
2 Department of Otolaryngology, An Nan Hospital, China Medical University, Tainan, 70965, Taiwan
3 Department of Cell Biology and Anatomy, College of Medicine, National Cheng Kung University, Tainan, 70101, Taiwan
4 Department of Medical Research, China Medical University Hospital, China Medical University, Taichung, 40402, Taiwan
* Corresponding Author: CHIA-YIH WANG. Email: email; BU-MIIN HUANG. Email: email
(This article belongs to the Special Issue: Navigating the Interplay of Cancer, Autophagy, ER Stress, Cell Cycle and Apoptosis: Mechanisms, Therapies, and Future Directions)

BIOCELL https://doi.org/10.32604/biocell.2024.050701

Received 14 February 2024; Accepted 25 March 2024; Published online 18 April 2024

Abstract

Background: 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. Methods: 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. Results: 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. Conclusions: Paclitaxel induced apoptosis through caspase cascade in KOSC3 cells.

Graphical Abstract

Paclitaxel induces human KOSC3 oral cancer cell apoptosis through caspase pathways

Keywords

Paclitaxel; Oral cancer; KOSC3 cells; Apoptosis; Caspase pathways

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