PT  - JOURNAL ARTICLE
AU  - Coffey, Robert J.
AU  - Goustin, Anton S.
AU  - Soderquist, Ann Mangelsdorf
AU  - Shipley, Gary D.
AU  - Wolfshohl, Jana
AU  - Carpenter, Graham
AU  - Moses, Harold L.
TI  - Transforming Growth Factor α and β Expression in Human Colon Cancer Lines: Implications for an Autocrine Model
DP  - 1987 Sep 01
TA  - Cancer Research
PG  - 4590--4594
VI  - 47
IP  - 17
4099  - http://cancerres.aacrjournals.org/content/47/17/4590.short
4100  - http://cancerres.aacrjournals.org/content/47/17/4590.full
SO  - Cancer Res1987 Sep 01; 47
AB  - Three human colon cancer lines (SW480, SW620, WIDR) secrete different levels of transforming growth factor β (TGFβ)-like and transforming growth factor α (TGFα)/epidermal growth factor (EGF)-like molecules into serum-free conditioned media as measured by competing activity in TGFβ and EGF radioreceptor assays. SW480 cells, the highest producers of TGFβ-like activity, lack detectable TGFβ receptors while SW620 cells, the highest producers of TGFα/EGF-like activity, lack EGF receptors. This study investigated the production of these growth factors at the mRNA level and examined the mechanism of loss of detectable receptors. Using complementary DNA probes for TGFβ and TGFα, it was demonstrated that mRNA levels correlated with the amounts of TGFβ and TGFα produced; TGFβ gene expression was highest in SW480 cells and TGFα gene expression was highest in SW620 cells. Acid washing of the SW480 cells prior to performing the TGFβ binding assay resulted in the unmasking of substantial levels of TGFβ receptors. Neither acid washing nor preincubation with suramin uncovered EGF receptors in SW620 cells. Also, and in contrast to the other two lines, EGF receptor expression could not be detected in SW620 cells by Northern gel analysis of receptor messenger RNA or by immunological analysis of receptor protein. Thus two distinct mechanisms (occupation of TGFβ receptor in SW480 cells, or absence of EGF receptor in SW620 cells) explain the lack of detectable TGFβ and EGF receptors in the binding assays. The autocrine hypothesis remains viable for TGFβ in SW480 cells but not for TGFα in SW620 cells; this would not discount a paracrine role in this latter case. ©1987 American Association for Cancer Research.