Open Access iconOpen Access

ARTICLE

crossmark

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 Authors: 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 2024, 48(7), 1047-1054. https://doi.org/10.32604/biocell.2024.050701

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


Cite This Article

APA Style
LAN, Y., CHENG, T., LEE, Y., WANG, C., HUANG, B. (2024). Paclitaxel induces human KOSC3 oral cancer cell apoptosis through caspase pathways. BIOCELL, 48(7), 1047-1054. https://doi.org/10.32604/biocell.2024.050701
Vancouver Style
LAN Y, CHENG T, LEE Y, WANG C, HUANG B. Paclitaxel induces human KOSC3 oral cancer cell apoptosis through caspase pathways. BIOCELL . 2024;48(7):1047-1054 https://doi.org/10.32604/biocell.2024.050701
IEEE Style
Y. LAN, T. CHENG, Y. LEE, C. WANG, and B. HUANG "Paclitaxel induces human KOSC3 oral cancer cell apoptosis through caspase pathways," BIOCELL , vol. 48, no. 7, pp. 1047-1054. 2024. https://doi.org/10.32604/biocell.2024.050701



cc This work is licensed under a Creative Commons Attribution 4.0 International License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
  • 734

    View

  • 220

    Download

  • 0

    Like

Share Link