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Taiwanin C elicits apoptosis in arecoline and 4‐nitroquinoline‐1‐oxide‐induced oral squamous cell carcinoma cells and hinders proliferation via epidermal growth factor receptor/PI3K suppression
Author(s) -
Tsai ChengYen,
Fang HsinYuan,
Shibu Marthandam Asokan,
Lin YuehMin,
Chou YungChen,
Chen YiHui,
Day CeciliaHsuan,
Shen ChiaYao,
Ban Bo,
Huang ChihYang
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.22742
Subject(s) - arecoline , cancer research , apoptosis , pi3k/akt/mtor pathway , cell growth , epidermal growth factor receptor , cell cycle , cancer , biology , protein kinase b , cell culture , cell cycle checkpoint , chemistry , medicine , receptor , biochemistry , genetics , muscarinic acetylcholine receptor
Oral Squamous Cell Carcinoma (OSSC) is a major life‐threatening disease with high incidence in the Southeast Asian countries. Chronic exposure to arecoline causes genetic changes in the epithelial cells of the oral mucosa, induces proliferation through activation of the EGF receptor and promotes downstream COX‐2 expression. Taiwanin C, a podophyllotoxin derived from Taiwania cryptomerioides Hayata is known to inhibit COX activity and to hinder PGE2 production in macrophages. In this study a tumor cell line T28 and a non‐tumor cell line N28 derived from mice OSCC models were used to study the effect of Taiwanin C on PGE 2 associated COX‐2 expression and cell cycle regulators. Taiwanin C activated p21 protein expression, down‐regulated cell cycle regulatory proteins, elevated apoptosis and down‐regulated p‐PI3K/p‐Akt survival mechanism in T28 oral cancer cells. Our results therefore emphasize the therapeutic potential of Taiwanin C against arecoline‐induced oral cancer.