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RESEARCH PRODUCT

Steroid-growth factor interaction in human prostate cancer. 1. Short-term effects of transforming growth factors on growth of human prostate cancer cells

Luigi CastagnettaRobin LeakeD. T. ChalmersFrank RinaldiCarmela SociGiuseppe CarrubaMichele Pavone-macalusoL. Comito

subject

Malemedicine.medical_specialtyTime Factorsmedicine.medical_treatmentClinical BiochemistryFluorescent Antibody Techniqueurologic and male genital diseasesBiochemistryProstate cancerEndocrinologyDU145Transforming Growth Factor betaInternal medicineLNCaPTumor Cells CulturedmedicineHumansReceptors Growth FactorEpidermal growth factor receptorMolecular BiologyPharmacologybiologyGrowth factorOrganic ChemistryProstatic NeoplasmsTransforming Growth Factor alphamedicine.diseaseAndrogen receptorEndocrinologyReceptors AndrogenCancer cellAndrogensbiology.proteinCell DivisionTransforming growth factor

description

In order to better define potential mechanisms of growth regulation in human prostate cancer cells, we have compared biological responses (such as short-term response to both transforming growth factor alpha and beta; TFG alpha and TFG beta) in relation to hormone sensitivity of LNCaP, DU145, and PC3 cells. Androgen receptor (AR) and epidermal growth factor receptor (EGF-R) content of each cell line was also investigated. In addition, expression of EGF, TGF alpha, and TGF beta was evaluated through immunofluorescent staining. Growth of androgen non-responsive PC3 cells was stimulated by TGF alpha (about 35%) and inhibited by TGF beta (more than 50%), with respect to controls, after 48 h exposure. Conversely, AR-positive, hormone-responsive LNCaP cells proved to be poorly sensitive, at least short-term, to either growth factor. Furthermore, high levels of both EGF-R and TGF alpha, and a fairly high amount of EGF, were found in DU145 cells and, to a lesser extent, in LNCaP cells; in contrast, PC3 cells exhibited low expression levels of both receptors (EGF-R) and ligands (EGF, TGF alpha), but displayed remarkable TGF beta binding and relatively high levels of endogenous TGF beta. Overall, these results suggest a differential sensitivity to TGF alpha and TGF beta by prostate cancer cells; TGF alpha response seems not to be proportional to the EGF-R content of individual cell lines.

https://doi.org/10.1016/0039-128x(94)90010-8