Abstract
We have previously shown that expression of gp200-MR6, a molecule that is functionally associated with the interleukin-4 receptor (IL-4R), is lost from breast carcinoma cells as malignancy increases. Here we have analysed a series of colorectal carcinoma cell lines and show a similar decrease with increasing malignancy. Moreover, analysis of the HRA-19 cell line, which can exhibit a poorly or a well-differentiated phenotype according to culture conditions, shows that gp200-MR6 is weakly expressed on the former but strongly expressed on the latter. Functional analysis using either IL-4 or monoclonal antibody (MAb) MR6 and the well-differentiated cell line SW1222 revealed that MAb MR6 acts as an agonist for IL-4, with both reagents causing a dose-dependent inhibition of cell division, but greatly enhancing the glandular differentiation of SW1222 in three-dimensional collagen gels. These observations suggest that the gp200-MR6 molecule may act as the product of a tumour suppressor gene and that its loss may be a primary event in tumourigenesis.
| Original language | English |
|---|---|
| Pages (from-to) | 605-611 |
| Number of pages | 7 |
| Journal | International Journal of Cancer |
| Volume | 71 |
| Issue number | 4 |
| DOIs | |
| Publication status | Published - 1997 |
| Externally published | Yes |
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ASJC Scopus subject areas
- Cancer Research
- Oncology
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Inhibition of growth and enhancement of differentiation of colorectal carcinoma cell lines by MAb MR6 and IL-4. / Al-Tubuly, Abdulhamid A.; Spijker, René; Pignatelli, Massimo; Kirkland, Suzan C.; Ritter, Mary A.
In: International Journal of Cancer, Vol. 71, No. 4, 1997, p. 605-611.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Inhibition of growth and enhancement of differentiation of colorectal carcinoma cell lines by MAb MR6 and IL-4
AU - Al-Tubuly, Abdulhamid A.
AU - Spijker, René
AU - Pignatelli, Massimo
AU - Kirkland, Suzan C.
AU - Ritter, Mary A.
PY - 1997
Y1 - 1997
N2 - We have previously shown that expression of gp200-MR6, a molecule that is functionally associated with the interleukin-4 receptor (IL-4R), is lost from breast carcinoma cells as malignancy increases. Here we have analysed a series of colorectal carcinoma cell lines and show a similar decrease with increasing malignancy. Moreover, analysis of the HRA-19 cell line, which can exhibit a poorly or a well-differentiated phenotype according to culture conditions, shows that gp200-MR6 is weakly expressed on the former but strongly expressed on the latter. Functional analysis using either IL-4 or monoclonal antibody (MAb) MR6 and the well-differentiated cell line SW1222 revealed that MAb MR6 acts as an agonist for IL-4, with both reagents causing a dose-dependent inhibition of cell division, but greatly enhancing the glandular differentiation of SW1222 in three-dimensional collagen gels. These observations suggest that the gp200-MR6 molecule may act as the product of a tumour suppressor gene and that its loss may be a primary event in tumourigenesis.
AB - We have previously shown that expression of gp200-MR6, a molecule that is functionally associated with the interleukin-4 receptor (IL-4R), is lost from breast carcinoma cells as malignancy increases. Here we have analysed a series of colorectal carcinoma cell lines and show a similar decrease with increasing malignancy. Moreover, analysis of the HRA-19 cell line, which can exhibit a poorly or a well-differentiated phenotype according to culture conditions, shows that gp200-MR6 is weakly expressed on the former but strongly expressed on the latter. Functional analysis using either IL-4 or monoclonal antibody (MAb) MR6 and the well-differentiated cell line SW1222 revealed that MAb MR6 acts as an agonist for IL-4, with both reagents causing a dose-dependent inhibition of cell division, but greatly enhancing the glandular differentiation of SW1222 in three-dimensional collagen gels. These observations suggest that the gp200-MR6 molecule may act as the product of a tumour suppressor gene and that its loss may be a primary event in tumourigenesis.
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UR - http://www.scopus.com/inward/citedby.url?scp=0030927775&partnerID=8YFLogxK
U2 - 10.1002/(SICI)1097-0215(19970516)71:4<605::AID-IJC16>3.0.CO;2-A
DO - 10.1002/(SICI)1097-0215(19970516)71:4<605::AID-IJC16>3.0.CO;2-A
M3 - Article
VL - 71
SP - 605
EP - 611
JO - International Journal of Cancer
JF - International Journal of Cancer
SN - 0020-7136
IS - 4
ER -