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| Content Provider | Journal of Biological Chemistry (JBC) |
|---|---|
| Author | Odajima, Junko Matsumura, Itaru Sonoyama, Junko Daino, Hanako Kawasaki, Akira Tanaka, Hirokazu Inohara, Naohiro Kitamura, Toshio Downward, Julian Nakajima, Koichi Hirano, Toshio Kanakura, Yuzuru |
| Abstract | Tyrosine kinase oncoproteins cause simultaneous activation of multiple intracellular signaling pathways. However, the precise mechanisms by which individual pathways induce oncogenesis are not well understood. We have investigated the roles of individual signaling pathways in v-Src-dependent cell growth and survival by inhibiting one particular pathway. v-Src induced constitutive activation of signal transducers and activators of transcription 3 (STAT3), phosphatidylinositol 3-kinase, and Ras in murine Ba/F3 cells and led to factor-independent proliferation. Dominant-negative mutants of STAT3 (STAT3D) and phosphatidylinositol 3-kinase (Δp85) inhibited v-Src-dependent growth by ∼60 and ∼40%, respectively. Moreover, dominant-negative Ras (N17) induced severe apoptosis, which was accompanied by down-regulation of Bcl-2 and activation of caspase-3. Although cells overexpressing Bcl-2 or caspase-3 inhibitors remained viable even when N17 was expressed, the growth was reduced by ∼85%. During N17- and STAT3D-induced growth suppression, expression of cyclin D2,cyclin D3, c-myc, and c-fos was suppressed by N17, whereas that of cyclin D2,cyclin E, and c-myc was suppressed by STAT3D. Thus, v-Src-activated Ras and STAT3 are involved in distinct but partly overlapping transcriptional regulation of cell cycle regulatory molecules. These results suggest that the full oncogenic activity of v-Src requires simultaneous activation of multiple signalings, in which Ras is particularly required for survival. |
| Related Links | http://www.jbc.org/content/275/31/24096.abstract |
| Ending Page | 24105 |
| Starting Page | 24096 |
| Page Count | 10 |
| File Format | HTM / HTML PDF |
| ISSN | 00219258 |
| Journal | Journal of Biological Chemistry (JBC) |
| Issue Number | 31 |
| Volume Number | 275 |
| DOI | 10.1074/jbc.M001606200 |
| e-ISSN | 1083351X |
| Language | English |
| Publisher | American Society for Biochemistry and Molecular Biology |
| Publisher Date | 2000-08-04 |
| Access Restriction | Open |
| Subject Keyword | Mitogen-activated protein kinase (MAPK) Signal transducers and activators of transcription (STAT) Phosphatidylinositol 3-kinase (PI3-K) Interleukin (IL) Antibody (Ab) Phosphotyrosine (PY) Isopropyl-β-d-thiogalactopyranoside (IPTG) Terminal deoxynucleotidyl-transferase-mediated biotin-dUTP nick end labeling (TUNEL) Lac repressor (LacR) MECHANISMS OF SIGNAL TRANSDUCTION |
| Alternative Title | Full Oncogenic Activities of v-Src Are Mediated by Multiple Signaling Pathways |
| Content Type | Text |
| Resource Type | Article |
| Subject | Cell Biology Biochemistry Molecular Biology |
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