Platelet-derived growth factor-stimulated c-myc RNA accumulation in MG-63 human osteosarcoma cells is independent of both protein kinase A and protein kinase C.
Platelet-derived growth factor-stimulated c-myc RNA accumulation in MG-63 human osteosarcoma cells is independent of both protein kinase A and protein kinase C.
复制标题
MG-63 人骨肉瘤细胞中血小板衍生生长因子刺激的 c-myc RNA 积累不依赖于蛋白激酶 A 和蛋白激酶 C。
DOI：
10.1128/mcb.10.1.184-192.1990
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发表时间：
1990
影响因子：
5.3
通讯作者：
Scher,CD
中科院分区：
文献类型：
--
作者：
Frick,KK;Scher,CD
Treatment of quiescent MG-63 cells with 12-0-tetradecanoylphorbol-13-acetate (TPA) or platelet-derived growth factor (PDGF) stimulates the rapid accumulation of c-mycRNA. We have now determined that a similar effect can be induced by cAMP. Treatment with forskolin (an activator of adenylate cyclase), IBMX (a phosphodiesterase inhibitor), PGE1, and isoproterenol stimulated accumulation of both cAMP and c-mycRNA, but no increase in either cAMP or c-mycRNA was seen with the inactive forskolin analog 1,9-dideoxyforskolin. Forskolin and IBMX acted synergistically in stimulating accumulation of both cAMP and c-mycRNA. However, three lines of evidence indicated that PDGF action is not mediated by cAMP. First, PDGF treatment caused no elevation of cAMP within 1 h, even in the presence of IBMX. Second, the kinetics of c-mycRNA elevation after treatment with PDGF or forskolin were similar, ruling out delayed onset of cAMP stimulation. Finally, simultaneous treatment with forskolin and the calcium ionophore A23187 enhanced the elevation of c-mycRNA levels; no such effect was seen with PDGF. We had previously shown that PDGF action is not affected by prior treatment of MG-63 cells with TPA, a treatment which desensitizes the c-mycresponse to TPA. Similarly, TPA pretreatment had minimal effect on forskolin or IBMX-induced c-mycexpression. These data suggest that cAMP, phorbol esters, and PDGF act independently to stimulatec-mycRNA expression in MG-63 cells. However, nuclear runoff experiments and RNA half-life measurements demonstrated that PDGF, phorbol ester, and cAMP all act to increase the transcription of theMYCgene.
