Synthesis of rhenium(I) and technetium(I) carbonyl/dithioether ligand complexes bearing 3,17β-estradiol

Reisgys, Martina; Wüst, F.; Alberto, Roger; Schibli, Roger; Schubiger, P. August; Pietzsch, Hans‐Jürgen; Spies, Hartmut; Johannsen, B.

doi:10.1016/s0960-894x(97)00396-x

Cited by 32 publications

(24 citation statements)

References 9 publications

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“…PTEN deletion is the most common event observed in prostate cancer cells (Reiss et al, 1992;Dupont et al, 2002;Stambolic, 2002). The loss of PTEN is thought to play an important role in tumor cell proliferation and metastasis, due to a lack of control of the signaling pathways that mediate cellular processes such as apoptosis and migration (Huang and Kontos, 2002;Kandel et al, 2002;Pene et al, 2002).…”

Section: Discussionmentioning

confidence: 99%

PTEN inhibits cell proliferation and induces apoptosis by downregulating cell surface IGF-IR expression in prostate cancer cells

et al. 2004

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PTEN is a tumor suppressor gene that is frequently mutated in human tumors. It functions primarily as a lipid phosphatase and plays a key role in the regulation of phosphatidylinositol-3 0 -kinase. PTEN appears to play a crucial role in modulating apoptosis by reducing the levels of PtdIns(3,4,5)P3, a phospholipid that activates AKT, a central regulator of apoptosis. To understand the role of PTEN in regulating cell proliferation and apoptosis, we stably overexpressed PTEN in PC3 cells, which are prostate cancer cells that lack PTEN. Overexpression of PTEN in two different clones inhibited cell proliferation and increased serum starvation-induced apoptosis, as compared to control cells. Interestingly, PTEN overexpression resulted in a 44-60% reduction in total insulinlike growth factor-I receptor (IGF-IR) protein levels and a 49-64% reduction in cell surface IGF-IR expression.[ 35 S]methionine pulse experiments in PC3 cells overexpressing PTEN demonstrated that these cells synthesize significantly lower levels of the IGF-IR precursor, whereas PTEN overexpression had no effect on IGF-IR degradation. Taken together, our results show that PTEN can regulate cell proliferation and apoptosis through inhibition of IGF-IR synthesis. These results have important implications for understanding the roles of PTEN and the IGF-IR in prostate cancer cell tumorigenesis.

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Section: Discussionmentioning

confidence: 99%

PTEN inhibits cell proliferation and induces apoptosis by downregulating cell surface IGF-IR expression in prostate cancer cells

et al. 2004

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“…The importance of type I IGF receptors in peripheral T cells function is also indicated by the fact that T cells can not enter the S-phase when the expression of type I IGF receptors is suppressed by anti-sense RNA [24]. Therefore, the differential expression of type I IGF receptor might reflect the different activation mechanisms for naive and memory cells [25,261, resulting in distinct cellular responses, e.g.…”

Section: Discussionmentioning

confidence: 99%

Differential expression of type I insulin‐like growth factor receptors in different stages of human T cells

et al. 1995

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Insulin-like growth factor I (IGF-I) has been implicated to play a regulatory role in T cell development and in T cell function. We investigated the expression of type I IGF receptors on human peripheral T cells related to the maturation and activation stage using the type I IGF receptor-specific monoclonal antibody alpha IR3. It appeared that 87% of the CD4+CD45RA+ cells and 66% of the CD8+CD45RA+ cells were alpha IR3+, whereas only 37% of the CD4+CD45R0+ cells and 38% of the CD8+CD45R0+ cells bound alpha IR3. We also found that the fraction of alpha IR3+ cells within in vivo or in vitro activated (HLA-DR+) T cells is markedly lower than in nonactivated (HLA-DR-) cells. In vitro phytohemagglutinin-activated T cells and CD4+CD45R0+ cells activated with recall antigens also contained less alpha IR3+ cells (1-6%) than nonactivated cells (30-54%).

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“…This observation may explain the lack of transformation by SV40 T antigen in IGF-1 receptor-deficient mice (24). Expression of c-Myb also increases the secretion of IGF-1 (25). In contrast, the Wilms' tumor gene, a tumor suppressor, has been reported to downregulate the expression of the IGF-1 receptor and IGF-2 (26).…”

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confidence: 97%

Suppression of Interleukin-1β-converting Enzyme-mediated Cell Death by Insulin-like Growth Factor

Jung

Miura²,

Yuan

1996

Journal of Biological Chemistry

109

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Synthesis of rhenium(I) and technetium(I) carbonyl/dithioether ligand complexes bearing 3,17β-estradiol

Cited by 32 publications

References 9 publications

PTEN inhibits cell proliferation and induces apoptosis by downregulating cell surface IGF-IR expression in prostate cancer cells

PTEN inhibits cell proliferation and induces apoptosis by downregulating cell surface IGF-IR expression in prostate cancer cells

Differential expression of type I insulin‐like growth factor receptors in different stages of human T cells

Suppression of Interleukin-1β-converting Enzyme-mediated Cell Death by Insulin-like Growth Factor

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