Myrcene exerts anti-tumor effects on oral cancer cells in vitro via induction of apoptosis

Purpose: To investigate the anticancer potential of myrcene against oral cancer cells.Methods: The effect of myrcene on oral cancer cell growth were studied using CCK-8 proliferation andclonogenic assays, while Annexin V-FITC/PI and DAPI staining methods were used for the determination of its effect...

Full description

Saved in:
Bibliographic Details
Published inTropical journal of pharmaceutical research Vol. 21; no. 5; pp. 933 - 938
Main Authors Wu, Zexiu, Li, Zhenmei, Liang, Yuan
Format Journal Article
LanguageEnglish
Published 16.06.2022
Online AccessGet full text

Cover

Loading…
More Information
Summary:Purpose: To investigate the anticancer potential of myrcene against oral cancer cells.Methods: The effect of myrcene on oral cancer cell growth were studied using CCK-8 proliferation andclonogenic assays, while Annexin V-FITC/PI and DAPI staining methods were used for the determination of its effect on cell apoptosis. Protein expression levels were assayed by western blotting technique. Wound healing and Transwell chamber assays were used to determine the effect of myrcene on oral cancer cell migration and invasion, respectively.Results: Myrcene significantly and dose-dependently inhibited oral cancer cell growth (p < 0.05). The anti-proliferative effect of myrcene was comparatively lower on Hs27 human fibroblast cells than on SCC9 oral cancer cells. Myrcene stimulated apoptosis in human oral cancer cells via enhancement of Bax expression and repression of Bcl-2 expression. The percentage of early and late apoptotic cells increased from 4.03 in untreated control to 27.77 when treated with 20 μM myrcene. Moreover, myrcene in vitro significantly suppressed the migration and invasion of oral cancer cells (p < 0.05).Conclusion: These results indicate that myrcene exerts potent anticancer effects on oral cancer cells via induction of apoptosis, and should be further investigated in vivo for this purpose.
ISSN:1596-5996
1596-9827
DOI:10.4314/tjpr.v21i5.4