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Ursolic acid induces apoptosis and autophagy in oral cancer cells
Author(s) -
Lin ChengWen,
Chin HsienKuo,
Lee ShouLun,
Chiu ChangFang,
Chung JingGung,
Lin ZiYin,
Wu ChiaYung,
Liu YingChen,
Hsiao YungTing,
Feng ChiaHsien,
Bai LiYuan,
Weng JingRu
Publication year - 2019
Publication title -
environmental toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.813
H-Index - 77
eISSN - 1522-7278
pISSN - 1520-4081
DOI - 10.1002/tox.22769
Subject(s) - autophagy , ursolic acid , apoptosis , pi3k/akt/mtor pathway , cancer research , protein kinase b , chemistry , p38 mitogen activated protein kinases , cancer cell , cancer , angiogenesis , mapk/erk pathway , microbiology and biotechnology , biology , pharmacology , signal transduction , medicine , biochemistry , chromatography
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.