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首页> 外文期刊>Biochemical and Biophysical Research Communications >MEK1-independent activation of MAPK and MEK1-dependent activation of p70 S6 kinase by stem cell factor (SCF) in ovarian cancer cells.
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MEK1-independent activation of MAPK and MEK1-dependent activation of p70 S6 kinase by stem cell factor (SCF) in ovarian cancer cells.

机译:卵巢癌细胞中干细胞因子(SCF)的MAPK的MEK1依赖性激活和p70 S6激酶的MEK1依赖性激活。

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We discovered a stem cell factor (SCF)-triggered, MEK1-independent, and PI3K-dependent MAPK activation pathway in the Kit-expressing ovarian cancer cell line HEY. When we knocked down MEK1 with RNA interference (RNAi) to study the function of MEK1 on the proliferation and survival of ovarian cancer cells, we found that impaired cell growth still occurred after MEK1 expression had been suppressed, although MAPK activation remained intact. This suggests that there is MEK1-independent activation of MAPK in the SCF-induced ovarian cancer cell growth process, and that MEK1 still plays a crucial role in maintaining the malignant properties of ovarian cancer cells even when it fails to activate MAPK as expected.
机译:我们在表达Kit的卵巢癌细胞系HEY中发现了由干细胞因子(SCF)触发的,不依赖MEK1和PI3K的MAPK激活途径。当我们用RNA干扰(RNAi)敲低MEK1来研究MEK1对卵巢癌细胞的增殖和存活的功能时,我们发现MEK1表达被抑制后,尽管MAPK激活仍然完整,但细胞生长仍然受损。这表明在SCF诱导的卵巢癌细胞生长过程中,MEK1的活化不依赖于MEK1,即使MEK1未能如预期的那样活化MAPK,MEK1仍在维持卵巢癌细胞的恶性特性中起着至关重要的作用。

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