Stem Cell Factor/c-kit Receptor Signaling Enhances the Proliferation and Invasion of Colorectal Cancer Cells Through the PI3K/Akt Pathway

Stem Cell Factor/c-kit Receptor Signaling Enhances the Proliferation and Invasion of Colorectal Cancer Cells Through the PI3K/Akt Pathway
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DOI:
10.1007/s10620-007-9759-7
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发表时间:
2007-04
影响因子:
3.1
通讯作者:
Akira Yasuda;H. Sawai;Hiroki Takahashi;N. Ochi;Y. Matsuo;H. Funahashi;Mikinori Sato;Y. Okada;H. Takeyama;T. Manabe
Akira Yasuda;H. Sawai;Hiroki Takahashi;N. Ochi;Y. Matsuo;H. Funahashi;Mikinori Sato;Y. Okada;H. Takeyama;T. Manabe
中科院分区:
医学3区
文献类型:
--
作者:
Akira Yasuda;H. Sawai;Hiroki Takahashi;N. Ochi;Y. Matsuo;H. Funahashi;Mikinori Sato;Y. Okada;H. Takeyama;T. Manabe

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在这项研究中,我们研究了c-kit受体(KIT)信号转导对大肠癌细胞增殖和侵袭的作用。RT-PCR、Western blot和流式细胞仪检测结果表明,c-kit在2株大肠癌细胞系中均有表达。在KIT阳性细胞系中,KIT被干细胞因子(SCF)激活。WST-1细胞增殖实验表明SCF能促进阳性细胞系的增殖。此外,SCF增强了KIT阳性细胞系的侵袭能力。Western blot显示SCF刺激可上调p44/42丝裂原活化蛋白激酶(MAPK)和Akt表达。我们研究了p44/42 MAPK和磷脂酰肌醇3-激酶(PI 3 K)/Akt通路在增殖和侵袭中所起的作用。PI 3 K/Akt活性与细胞增殖和侵袭密切相关,而p44/42 MAPK仅与细胞侵袭相关。结论:SCF增强KIT阳性结直肠癌细胞的增殖和侵袭主要通过PI 3 K/Akt途径实现。
In this study, we examined the role of c-kitreceptor (KIT) signal transduction on the proliferation and invasion of colorectal cancer cells. We found that c-kitwas expressed in 2 colorectal cancer cell lines as determined by RT-PCR, Western blot, and flow cytometry. In KIT-positive lines, KIT was activated by stem cell factor (SCF). SCF enhanced cellular proliferation of positive lines as demonstrated by the WST-1 proliferation assay. Furthermore, SCF enhanced the invasive ability of KIT-positive cell lines. SCF stimulation upregulated p44/42 mitogen-activated protein kinase (MAPK) and Akt as shown by Western blot. We examined the roles played by p44/42 MAPK and phosphatidylinositol 3-kinase (PI3K)/Akt pathways in proliferation and invasion. PI3K/Akt activity strongly correlated with proliferation and invasion and p44/42 MAPK was correlated with only invasion. In conclusion, the SCF-enhanced proliferation and invasion of KIT-positive colorectal cancer cells is achieved mainly through the PI3K/Akt pathway.