| Title | CMTM8 induces caspase-dependent and -independent apoptosis through a mitochondria-mediated pathway |
| Authors | Jin, Caining Wang, Ying Han, Wenling Zhang, Yingmei He, Qihua Li, Dan Yin, Caihua Tian, Linjie Liu, Dazhen Song, Quanshen Ma, Dalong |
| Affiliation | Peking Univ, Sch Basic Med Sci, Lab Med Immunol, Beijing 100083, Peoples R China. Peking Univ, Ctr Human Dis Genom, Beijing 100083, Peoples R China. Peking Univ, Hlth & Med Anal Ctr, Beijing 100083, Peoples R China. Peking Univ, Sch Basic Med Sci, Lab Med Immunol, 38 xueyuan Rd, Beijing 100083, Peoples R China. |
| Keywords | GROWTH-FACTOR RECEPTOR MONOCLONAL-ANTIBODY TYROSINE KINASE PANCREATIC-CANCER CYTOCHROME-C INDUCTION INHIBITION PROTEIN CELLS DEATH |
| Issue Date | 2007 |
| Publisher | 细胞生理学杂志 |
| Citation | JOURNAL OF CELLULAR PHYSIOLOGY.2007,211,(1),112-120. |
| Abstract | The mitochondria-mediated apoptotic pathway is regulated by members of the Bcl-2 family. Epidermal growth factor (EGF) induces Bad phosphorylation at Ser(112) via mitogen-activated protein kinase (MAPK), impairing its binding to Bcl-2 and Bcl-xL and interfering with their anti-apoptotic functions. In the current study, we utilized Western blot, immunofluorescence, flow cytometry, and confocal microscopy to examine the effects of CMTM8 overexpression on apoptosis. Our data indicated levels of Bad-S-112 phosphorylation were lower in CMTM8-transfected cells compared to pCDB-transfected cells. Caspase-dependent and independent mediated apoptosis, induced by CMTM8 overexpression, was facilitated by the mitochondria and inhibited by knockdown of Bad or overexpression of Bcl-xL. Previous research in our laboratory also demonstrated CMTM8 attenuated EGFR-mediated signaling pathways by decreasing ERK1/2phosphorylation levels. These data implicate CMTM8 as a negative regulator of EGF-induced signaling, with potential use as a novel therapeutic gene for EGFR-targeted anticancer gene therapy. |
| URI | http://hdl.handle.net/20.500.11897/198568 |
| ISSN | 0021-9541 |
| DOI | 10.1002/jcp.20914 |
| Indexed | SCI(E) PubMed |
| Appears in Collections: | 基础医学院 |
