Absence of transforming growth factor-β responsiveness in the tamoxifen growth-inhibited human breast cancer cell line CAMA-1

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Abstract
Tamoxifen has been an effective antiestrogen in suppressing breast cancer growth which is estrogen‐responsive or dependent. Early studies have provided circumstantial evidence that transforming growth factor‐β (TGF‐β) may be an autocrine mediator of tamoxifen action. Therefore, it is both fundamentally important and clinically relevant to investigate the relationship between tamoxifen and TGF‐β. In this study, we demonstrated that CAMA‐1 cells, which are sensitive to tamoxifen inhibition, did not respond to TGF‐β growth inhibition. The type I and II TGF‐β receptors were undetectable by the radio‐ligand affinity labeling technique. Despite the presence of a normal TGF‐β type II receptor gene, the mRNA transcript of the gene was undetectable by the extremely sensitive Intron‐differential RNA/PCR method. The possibility that the lack of TGF‐β receptors might be intimately linked to the absence of normal retinoblastoma (Rb) gene products, as suggested by previous studies of retinoblastoma cells, was further investigated. The lack of TGF‐β receptor expression was found due to reasons other than the absence, deletion or abnormality of the Rb gene because a normal Rb gene and its hyper‐ and hypo‐phosphorylated protein products were detected in CAMA‐1 cells. In conclusion, our results suggest that the TGF‐β system is not obligatory for antiestrogen growth inhibition of CAMA‐1 cells.