Stem cell factor/c-kit receptor signaling enhances the proliferation and invasion of colorectal cancer cells through the PI3K/Akt Pathway
Digestive Diseases and Sciences, ISSN: 0163-2116, Vol: 52, Issue: 9, Page: 2292-2300
2007
- 59Citations
- 25Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations59
- Citation Indexes59
- 59
- CrossRef38
- Captures25
- Readers25
- 25
Article Description
In this study, we examined the role of c-kit receptor (KIT) signal transduction on the proliferation and invasion of colorectal cancer cells. We found that c-kit was 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. © 2007 Springer Science+Business Media, LLC.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=34547830309&origin=inward; http://dx.doi.org/10.1007/s10620-007-9759-7; http://www.ncbi.nlm.nih.gov/pubmed/17410437; http://link.springer.com/10.1007/s10620-007-9759-7; https://dx.doi.org/10.1007/s10620-007-9759-7; https://link.springer.com/article/10.1007/s10620-007-9759-7; http://www.springerlink.com/index/10.1007/s10620-007-9759-7; http://www.springerlink.com/index/pdf/10.1007/s10620-007-9759-7
Springer Science and Business Media LLC
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