CREB, a possible upstream regulator of Bcl-2 in trichosanthin-induced HeLa cell apoptosis.
Our previous reports indicated that cyclic AMP response element-binding (CREB) protein was involved in the regulation of Bcl-2 expression in apoptotic HeLa cells induced by trichosanthin (TCS). Here we presented that blockade the binding site of CREB to Bcl-2 by a CRE decoy oligonucleotide abrogated the TCS-decreased Bcl-2 expression. Furthermore, overexpression of phosphorylated CREB (p-CREB) in cells transfected with p-CREB/GFP fusion construct resulted in an increase of Bcl-2 protein content, however, this increase was attenuated by TCS treatment. Therefore, this data supports the hypothesis that CREB is a possible upstream regulator of Bcl-2 in apoptotic HeLa cells induced by TCS. The study provides new insights into understanding the mechanism of TCS in the treatment of cervical cancer.
Wang
Ping
P
Medical School, Ningbo University, 315211, Ningbo, China. pinoav@hotmail.com
Xu
Jin
J
Zhang
Cheng
C
D017209:Apoptosis / Q000187:drug effects*; D049109:Cell Proliferation / Q000187:drug effects; D017362:Cyclic AMP Response Element-Binding Protein / Q000378:metabolism*; D053938:DNA Fragmentation / Q000187:drug effects; D006367:HeLa Cells; D006801:Humans; D010766:Phosphorylation / Q000187:drug effects; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism*; D015978:Trichosanthin / Q000494:pharmacology*; D015854:Up-Regulation / Q000187:drug effects
C115163:CREB1 protein, human; D017362:Cyclic AMP Response Element-Binding Protein; D019253:Proto-Oncogene Proteins c-bcl-2; D015978:Trichosanthin