Hormonal regulation of transforming growth factor β-2 expression in human prostate cancer

Knabbe, Cornelius; Klein, H.; Zugmaier, Gerhard; Voigt, Kai‐Ingo

doi:10.1016/0960-0760(93)90067-7

Cited by 35 publications

(21 citation statements)

References 16 publications

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“…Although a number of studies have been published on the relationship between TGF-␤1 and prostate cancer, there are only limited and conflicting reports on the association of TGF-␤2 and prostate cancer, despite the fact that it was originally purified from prostate cancer cells. A few studies have shown that TGF-␤2 mRNA and protein are overproduced by the prostate cancer cell lines, PC-3 and LNCaP (27,28), yet others have shown that TGF-␤2 mRNA levels remain unchanged in prostate cancer (28,29). When patients with prostate cancer were grouped by pathological stage or Gleason grade, plasma TGF-␤2 levels were higher in patients with low pathological stages and low-grade disease.…”

Section: Discussionmentioning

confidence: 99%

Gene Expression of Angiogenic Factors Correlates with Metastatic Potential of Prostate Cancer Cells

et al. 2004

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Section: Discussionmentioning

confidence: 99%

Gene Expression of Angiogenic Factors Correlates with Metastatic Potential of Prostate Cancer Cells

et al. 2004

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“…In general, TGF 1 stimulates mesenchyme and inhibits epithelial growth . TGF 1 and TGF 2 have been identified in human prostate and implicated in prostatic disease (Knabbe et al 1993, Truong et al 1993. Addition of TGF 1 to cultured prostatic epithelial and stromal cells has been reported to inhibit proliferation in both cell types (Sutkowski et al 1992).…”

Section: Introductionmentioning

confidence: 99%

Transforming growth factor-beta1 up-regulates p15, p21 and p27 and blocks cell cycling in G1 in human prostate epithelium

Robson¹,

Gnanapragasam²,

Byrne³

et al. 1999

Journal of Endocrinology

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Transforming growth factor-1 (TGF 1) is inhibitory to most epithelia, but its role in the control of proliferation of prostatic epithelium is unclear. In some cells, TGF 1 inhibition is achieved by up-regulation of cyclindependent kinase (cdk) inhibitors including p15, p21 and p27.Our aims were to determine whether the effects of TGF 1 on human prostatic epithelial cell cycle kinetics were mediated by alterations in the levels of the cdk inhibitors p15, p16, p21 and p27 and hypophosphorylated retinoblastoma protein (Rb).Human prostatic epithelial cells in primary culture were grown in the presence of TGF 1 (0-10 ng/ml) for up to 4 days and proliferation assessed using a [ 3 H]thymidine uptake assay. Levels of p15, p16, p21 and p27 were measured at both mRNA and protein level by means of a reverse transcriptase PCR-based assay and Western analysis. Rb and cdk2 levels were measured.Exogenous TGF 1 (0-5 ng/ml) inhibited proliferation. This was associated with blocking of the cell cycle at G1, and up to 4-fold increases in p15, p21 and p27 mRNA levels, but no change was observed in p16 mRNA levels; these changes were not blocked by cycloheximide. Increased levels of p15, p21 and p27 protein were also accompanied by increased levels of hypo-phosphorylated Rb and decreased cdk2 kinase activity.TGF 1 has mainly inhibitory effects on benign human prostatic epithelium, which are caused by up-regulation of cdk inhibitors, hypo-phosphorylation of Rb and delaying of the cell cycle in G1.

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“…The increase in Tgfb2 expression in the bones of mOBLARKOs is consistent with the increased bone mineral matrix and mineralization in these mice. A possible role of androgens via the AR in the regulation of Tgfb2 expression is supported by the observation that androgen withdrawal increases Tgfb2 mRNA in LNCap cells (Knabbe et al 1993).…”

Section: Discussionmentioning

confidence: 49%

Identification of gene pathways altered by deletion of the androgen receptor specifically in mineralizing osteoblasts and osteocytes in mice

Russell¹,

Clarke²,

Skinner³

et al. 2012

Journal of Molecular Endocrinology

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Androgens play a key role in skeletal growth and maintenance in males and can mediate their actions, at least in part, via the androgen receptor (AR) in osteoblasts. To investigate the mechanisms by which androgens exert their effects via the AR in mineralizing osteoblasts and osteocytes, we identified gene targets/pathways regulated by the AR using targeted gene expression and microarray approaches on bone isolated from mice in which the AR is specifically deleted in mineralizing osteoblasts and osteocytes (mOBL-ARKOs). Gene ontology mining indicated a number of biological processes to be affected in the bones of mOBL-ARKOs including skeletal and muscular system development and carbohydrate metabolism. All genes identified to have altered expression in the bones of mOBL-ARKOs were confirmed by Q-PCR for their androgen responsiveness in an androgen deprivation and replacement mouse model. The osteoblast genes Col1a1 and Bglap and the osteoclast genes Ctsk and RANKL (Tnfs11) were upregulated in the bones of mOBLARKOs, consistent with the increased matrix synthesis, mineralization, and bone resorption observed previously in these mice. Of significant interest, we identified genes involved in carbohydrate metabolism (adiponectin and Dpp4) and in growth and development (GH, Tgfb (Tgfb2), Wnt4) as potential targets of androgen action via the AR in mineralizing osteoblasts.

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Hormonal regulation of transforming growth factor β-2 expression in human prostate cancer

Cited by 35 publications

References 16 publications

Gene Expression of Angiogenic Factors Correlates with Metastatic Potential of Prostate Cancer Cells

Gene Expression of Angiogenic Factors Correlates with Metastatic Potential of Prostate Cancer Cells

Transforming growth factor-beta1 up-regulates p15, p21 and p27 and blocks cell cycling in G1 in human prostate epithelium

Identification of gene pathways altered by deletion of the androgen receptor specifically in mineralizing osteoblasts and osteocytes in mice

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