Thrombospondin 1: a multifunctional protein implicated in the regulation of tumor growth

Sid, Brice; Sartelet, Hervé; Bellon, Georges; Btaouri, Hassan El; Rath, Géraldine; Delorme, N; Haye, Bernard; Martiny, Laurent

doi:10.1016/j.critrevonc.2003.09.009

Cited by 93 publications

(76 citation statements)

References 130 publications

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“…2B). With respect to regulation of proliferation and apoptosis, the CD36 receptor ligand thrombospondin 1 presents both stimulatory and inhibitory effects (25). As observed in PC12 cells, increased expression of SPHK1 resulted in increases of sphingosine-1-phosphate levels and marked suppression of apoptosis (26).…”

Section: Discussionmentioning

confidence: 95%

213Bi-induced death of HSC45-M2 gastric cancer cells is characterized by G2 arrest and up-regulation of genes known to prevent apoptosis but induce necrosis and mitotic catastrophe

Seidl¹,

Port

Gilbertz

et al. 2007

Molecular Cancer Therapeutics

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Tumor cells are efficiently killed after incubation with A-emitter immunoconjugates targeting tumor-specific antigens. Therefore, application of A-emitter immunoconjugates is a promising therapeutic option for treatment of carcinomas that are characterized by dissemination of single tumor cells in the peritoneum like ovarian cancer or gastric cancer. In diffuse-type gastric cancer, 10% of patients express mutant d9-E-cadherin on the surface of tumor cells that is targeted by the monoclonal antibody d9MAb. Coupling of the A-emitter 213 Bi to d9MAb provides an efficient tool to eliminate HSC45-M2 gastric cancer cells expressing d9-E-cadherin in vitro and in vivo. Elucidation of the molecular mechanisms triggered by A-emitters in tumor cells could help to improve strategies of A-emitter radioimmunotherapy. For that purpose, gene expression of 213 Bi-treated tumor cells was quantified using a real time quantitative-PCR low-density array covering 380 genes in combination with analysis of cell proliferation and the mode of cell death. We could show that 213 Bi-induced cell death was initiated by G 2 arrest; up-regulation of tumor necrosis factor (TNF), SPHK1, STAT5A, p21, MYT1, and SSTR3; and down-regulation of SPP1, CDC25 phosphatases, and of genes involved in chromosome segregation. Together with morphologic changes, these results suggest that 213 Bi activates death cascades different from apoptosis. Furthermore, 213 Bitriggered up-regulation of SSTR3 could be exploited for improvement of the therapeutic regimen. [Mol Cancer Ther 2007;6(8):2346 -59]

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Section: Discussionmentioning

confidence: 95%

213Bi-induced death of HSC45-M2 gastric cancer cells is characterized by G2 arrest and up-regulation of genes known to prevent apoptosis but induce necrosis and mitotic catastrophe

Seidl¹,

Port

Gilbertz

et al. 2007

Molecular Cancer Therapeutics

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“…Amphiregulin is the major EGF receptor ligand active during pubertal mammary ductal outgrowth in the mouse (Kenney et al, 1995(Kenney et al, , 1996Luetteke et al, 1999) and its expression has been shown to be regulated by estrogen (Martinez-Lacaci et al, 1995;Soulez and Parker, 2001). Thrombospondin-1 is an adhesive glycoprotein component of the extracellular matrix (Sid et al, 2004). It binds and activates latent TGFb (Negoescu et al, 1995;Munger et al, 1997).…”

Section: Cited1 In the Pubertal Mammary Gland J Howlin Et Almentioning

confidence: 99%

CITED1 homozygous null mice display aberrant pubertal mammary ductal morphogenesis

et al. 2005

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“…Angiogenesis is essential for rapid growth of solid tumors, because it increases vascularization of tissues adjacent to the tumor, thereby increasing the supply of nutrients to rapidly proliferating tumor cells (Folkman 1995, Bergers & Benjamin 2003, Sid et al 2004. This suggests that it may be possible to reduce the supply of nutrients, and thereby slow or prevent tumor growth, by inhibiting angiogenesis.…”

Section: Introductionmentioning

confidence: 99%

Regulation of thrombospondin-1 by natural and synthetic progestins in human breast cancer cells

Hyder¹,

Liang²,

Wu³

et al. 2009

Endocrine-Related Cancer

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Our recent studies show that progestins induce vascular endothelial growth factor (VEGF) in breast cancer cells that express mutant p53 protein. Here, we show that natural and synthetic progestins also induce thrombospondin-1 (TSP-1) mRNA and protein in T47-D and BT-474 breast cancer cells. Antiprogestin RU-486 inhibits the induction of VEGF and TSP-1 by progestins, suggesting that this effect of progestin is mediated by the progesterone receptor (PR). Actinomycin-D, but not puromycin, also blocks progestin-dependent induction of TSP-1. A putative progestin-response element was identified in the human TSP-1 promoter, which is consistent with the hypothesis that a progestin-PR complex might directly regulate transcription of the TSP-1 gene in human cells. Conditioned medium from progestin-treated breast cancer cells stimulates endothelial cell proliferation in the absence though not in the presence of antibody to TSP-1, indicating that TSP-1 secreted by breast cancer cells could be pro-angiogenic. Since tumor cell-derived TSP-1 has the potential to promote angiogenesis in the tumor microenvironment, it could be a potential target for breast cancer therapy.

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Thrombospondin 1: a multifunctional protein implicated in the regulation of tumor growth

Cited by 93 publications

References 130 publications

213Bi-induced death of HSC45-M2 gastric cancer cells is characterized by G2 arrest and up-regulation of genes known to prevent apoptosis but induce necrosis and mitotic catastrophe

213Bi-induced death of HSC45-M2 gastric cancer cells is characterized by G2 arrest and up-regulation of genes known to prevent apoptosis but induce necrosis and mitotic catastrophe

CITED1 homozygous null mice display aberrant pubertal mammary ductal morphogenesis

Regulation of thrombospondin-1 by natural and synthetic progestins in human breast cancer cells

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