Switch to
| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
1
|
| pubmed:dateCreated |
1997-7-24
|
| pubmed:abstractText |
Activation of the receptor tyrosine kinase c-kit by the kit-ligand, also known as stem cell factor (SCF), is essential to melanocyte and germ cell development and during the early stages of hematopoiesis. Deregulated expression of c-kit has been reported in malignancies affecting these lineages, i.e., myeloid leukemias, melanomas, and germ cell tumors. In addition, c-kit and SCF are coexpressed in some breast and colorectal cancer (CRC) cells, raising the question of whether c-kit serves an autocrine role in normal or malignant epithelial tissues. In this study, we demonstrate that human colorectal carcinomas, but not normal colorectal mucosa cells, coexpress SCF and c-kit in situ. Expression of c-kit was also observed in mucosa adjacent to colorectal tumor tissue. Consistent with a growth-regulatory role of SCF in CRC cells, exogenous SCF stimulated anchorage-dependent and anchorage-independent growth in four out of five CRC cell lines. Exogenous transforming growth factor (TGF)-beta 1 added at nanomolar concentrations to HT-29 CRC cells, which express the type I, II, and III TGF-beta receptors, downregulated c-kit expression to background levels and inhibited c-kit-dependent proliferation. Similarly, TGF-beta 1 inhibited SCF-dependent proliferation of three first-passage CRC cell lines. In summary, expression of the potential autocrine SCF/ c-kit axis is a tumor-associated phenomenon in colorectal cancer that can be suppressed by TGF-beta 1 in TGF-beta-responsive CRC cells.
|
| pubmed:grant | |
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-kit,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Neoplasm,
http://linkedlifedata.com/resource/pubmed/chemical/Stem Cell Factor,
http://linkedlifedata.com/resource/pubmed/chemical/Transforming Growth Factor beta
|
| pubmed:status |
MEDLINE
|
| pubmed:month |
Jul
|
| pubmed:issn |
0021-9541
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
172
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
1-11
|
| pubmed:dateRevised |
2009-11-19
|
| pubmed:meshHeading |
pubmed-meshheading:9207920-Adult,
pubmed-meshheading:9207920-Aged,
pubmed-meshheading:9207920-Carcinoma,
pubmed-meshheading:9207920-Cell Adhesion,
pubmed-meshheading:9207920-Cell Division,
pubmed-meshheading:9207920-Colorectal Neoplasms,
pubmed-meshheading:9207920-Down-Regulation,
pubmed-meshheading:9207920-Female,
pubmed-meshheading:9207920-Gene Expression Regulation, Neoplastic,
pubmed-meshheading:9207920-Humans,
pubmed-meshheading:9207920-Intestinal Mucosa,
pubmed-meshheading:9207920-Male,
pubmed-meshheading:9207920-Middle Aged,
pubmed-meshheading:9207920-Proto-Oncogene Proteins c-kit,
pubmed-meshheading:9207920-RNA, Messenger,
pubmed-meshheading:9207920-RNA, Neoplasm,
pubmed-meshheading:9207920-Stem Cell Factor,
pubmed-meshheading:9207920-Transforming Growth Factor beta
|
| pubmed:year |
1997
|
| pubmed:articleTitle |
Growth stimulation of colorectal carcinoma cells via the c-kit receptor is inhibited by TGF-beta 1.
|
| pubmed:affiliation |
Department of Clinical Physiopathology, University of Torino, Italy. robini@mbox.vol.it
|
| pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
|