Ursolic acid induces apoptosis and autophagy in oral cancer cells

Oral squamous cell carcinoma (OSCC) is the fifth common cause of cancer mortality in Taiwan with high incidence and recurrence and needs new therapeutic strategies. In this study, ursolic acid (UA), a triterpenoid, was examined the antitumor potency in OSCC cells. Our results showed that UA inhibite...

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Bibliographic Details
Published in:Environmental toxicology 2019-09, Vol.34 (9), p.983-991
Main Authors: Lin, Cheng‐Wen, Chin, Hsien‐Kuo, Lee, Shou‐Lun, Chiu, Chang‐Fang, Chung, Jing‐Gung, Lin, Zi‐Yin, Wu, Chia‐Yung, Liu, Ying‐Chen, Hsiao, Yung‐Ting, Feng, Chia‐Hsien, Bai, Li‐Yuan, Weng, Jing‐Ru
Format: Article
Language:English
Subjects:
AKT protein
Angiogenesis
Angiogenesis Inhibitors - pharmacology
Antitumour agents
Apoptosis
Apoptosis - drug effects
Autophagy
Autophagy - drug effects
Biomarkers
Cancer
Carcinoma, Squamous Cell - metabolism
Carcinoma, Squamous Cell - pathology
Caspase
Cell Line, Tumor
Cell proliferation
Cell Proliferation - drug effects
Cells
Down-Regulation
Humans
invasion
Mouth Neoplasms - metabolism
Mouth Neoplasms - pathology
Neoplasms
NF-kappa B - metabolism
Oral cancer
Oral squamous cell carcinoma
OSCC
Phagocytosis
Phagosomes
Proliferation
Secretion
Signal Transduction
Squamous cell carcinoma
Time dependence
TOR protein
Triterpenes - pharmacology
Ursolic Acid
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Summary:Oral squamous cell carcinoma (OSCC) is the fifth common cause of cancer mortality in Taiwan with high incidence and recurrence and needs new therapeutic strategies. In this study, ursolic acid (UA), a triterpenoid, was examined the antitumor potency in OSCC cells. Our results showed that UA inhibited the proliferation of OSCC cells in a dose‐ and time‐dependent manner in both Ca922 and SCC2095 oral cancer cells. UA induced caspase‐dependent apoptosis accompanied with the modulation of various biological biomarkers including downregulating Akt/mTOR/NF‐κB signaling, ERK, and p38. In addition, UA inhibited angiogenesis as evidenced by abrogation of migration/invasion and blocking MMP‐2 secretion in Ca922 cells. Interestingly, UA induced autophagy in OSCC cells, as manifested by LC3B‐II conversion and increased p62 expression and accumulation of autophagosomes. Inhibition by autophagy inhibitor enhanced UA‐mediated apoptosis in Ca922 cells. The experiment provides a rationale for using triterpenoid in the treatment of OSCC.
ISSN:1520-4081
1522-7278
DOI:10.1002/tox.22769