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Induction of laryngeal cancer cell death by Ent‐11‐hydroxy‐15‐oxo‐kaur‐16‐en‐19‐oic acid
Author(s) -
Vlantis Alexander C.,
Lo Chun Shan,
Chen George G.,
Ci Liang Nian,
Lui Vivian W. Y.,
Wu Kefeng,
Deng Yi Feng,
Gong Xianling,
Lu Yingnian,
Tong Michael C. F.,
van Hasselt C. Andrew
Publication year - 2010
Publication title -
head and neck
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.012
H-Index - 127
eISSN - 1097-0347
pISSN - 1043-3074
DOI - 10.1002/hed.21357
Subject(s) - apoptosis , annexin , programmed cell death , poly adp ribose polymerase , microbiology and biotechnology , cancer cell , chemistry , cell , cancer , cancer research , biology , biochemistry , polymerase , dna , genetics
Background. Ent‐11‐hydroxy‐15‐oxo‐kaur‐16‐en‐19‐oic acid (5F) is known to exhibit antitumor activity, but its mechanism is not completely understood. 5F has not been tested in laryngeal cancer. Methods. Two laryngeal cancer cell lines were treated with 5F. Cell death was analyzed by MTT [3‐(4,5‐dimethylthiozol‐2‐yl)‐2,5‐diphenyltetrazolium bromide] and Annexin V assay. Nuclear factor kappa beta (NF‐κB)– and apoptosis‐related molecules were examined. Results. 5F induced laryngeal cancer cell death in a dose‐dependent manner. The Annexin V assay and the measurement of cleavage of procaspase‐3 and poly(ADP‐ribose) polymerase demonstrated that the 5F‐induced cell death was mainly apoptotic. 5F slightly reduced the basal level of NF‐κB, but significantly suppressed the inducible NF‐κB by reducing its transcriptional activity, protecting its inhibitory subunit IκBα from degradation, and suppressing its level in the nucleus. 5F also inhibited pro‐proliferative and anti‐apoptotic molecules but promoted pro‐apoptotic Bax. Conclusions. 5F induces apoptosis of laryngeal cancer cells by inhibiting NF‐κB activation/induction, suppressing pro‐proliferative and anti‐apoptotic molecules, and promoting pro‐apoptotic Bax. © 2010 Wiley Periodicals, Inc. Head Neck, 2010