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本帖最后由 kevinloplp 于 2011-1-13 00:03 编辑 . p/ Y( `- c: ?, S4 s6 K7 c
2 E7 R4 z6 L8 t j/ YThe survival of IL-6-dependent myeloma cells critically relies on their capability to transit the G1 to S phase interval of the cell cycle.) v: z4 G$ D- v9 V- E, J
! e2 O) ?$ Q% b# g( ^Côté S, Lemieux R, Simard C.4 O. \8 @7 x. c4 _- @* F
4 _6 B3 s$ ~! t9 P {Département de Recherche et Développement, Héma-Québec, Sainte-Foy, QC, Canada. scote@hema-quebec.qc.ac
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Cell Signal. 2005 May;17(5):615-24.
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. e! V1 V4 j0 |5 V) QAbstract
- E9 T& _0 W0 v0 o+ r2 nInterleukin-6 (IL-6) has an essential role in the initial progression of myeloma cell tumours. IL-6 triggers proliferation of these cells via the Ras-mitogen-activated protein kinase (MAPK) cascade and is thought to promote their survival via signal transducer and activator of transcription (STAT) pathway-dependent regulation of Bcl-2 family antiapoptotic members. Using IL-6-dependent murine B9 hybridoma/plasmacytoma cells, we here report that exiting the cell cycle G1 phase is a crucial step contributing to maintain viability. We show that (1) drug-mediated reversible G1 arrest triggered apoptosis despite the presence of IL-6; (2) a short IL-6 pulse to G1-arrested cells was sufficient to induce S phase entry and prevent apoptosis; and (3) phorbol ester and related derivatives promoted S phase entry and survival of IL-6-starved cells without up-regulating bcl-XL expression. Furthermore, that the MAPK kinase (MEK) 1/2 inhibitor, U0126, blocked proliferation and induced death of B9 cells indicate that IL-6 may not exert its survival effect primarily through bcl-XL and emphasizes the key role of Ras-MAPK cascade elements in the regulation of myeloma growth/viability.
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PMID: 15683736 [PubMed - indexed for MEDLINE]1 d" W" {) `! Y! K5 `" }5 M
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谢谢 偶的邮箱：kevin_zyf@126.com |
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发表于 2011-1-12 23:59
