The snake venom disintegrin salmosin induces apoptosis by disassembly of focal adhesions in bovine capillary endothelial cells

Hong, So Yeon; Lee, Hyeryung; You, Weon Kyoo; Chung, Kyeong Woo; Kim, Doo Sik; Song, Kiwon

doi:10.1016/s0006-291x(03)00213-4

Cited by 44 publications

(27 citation statements)

References 27 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Saxatilin, isolated from a Korean snake (Gloydius saxatilis), has been shown to inhibit platelet aggregation, human umbilical vein endothelial cell proliferation, and smooth muscle cell migration (31). Salmosin, a disintegrin purified from a Korean snake (Agkistrodon halys brevicaudus) venom, interacts with integrin a(v)h(3) and induces apoptotic cell death by competing with the extracellular matrix for direct binding to integrin a(v)h(3) on the cell surface (33). Thus, our present findings, which showed the in vitro anticancer efficacy of SVT and mechanistic rationale (cell cycle arrest and apoptosis induction) against advanced human prostate cancer cells, warrant further in vivo efficacy studies in preclinical human prostate cancer models, as well as the estimation of pharmacologically achievable doses having biological significance in in vitro studies.…”

Section: Discussionmentioning

confidence: 99%

Inhibitory effect of snake venom toxin from Vipera lebetina turanica on hormone-refractory human prostate cancer cell growth: induction of apoptosis through inactivation of nuclear factor κB

Son¹,

Park²,

Chae

et al. 2007

Molecular Cancer Therapeutics

View full text Add to dashboard Cite

We investigated whether the snake venom toxin (SVT) from Vipera lebetina turanica inhibits cell growth of human prostate cancer cells by inducing apoptosis and also studied possible signaling pathways involved in this cell death. SVT inhibited growth of PC-3 and DU145 cells, androgen-independent prostate cancer cells, but not LNCaP cells, a human androgen-dependent prostate cancer cell. Cells were arrested in the G 2 -M phase by SVT with a concomitant decrease in the expression of the G 2 -M phase regulatory protein cyclin B1 and were also arrested in the G 1 -S phase with decreasing expression of cyclin-dependent kinase 4, cyclin D1 and cyclin E. In addition to the growth-inhibitory effect, SVT increased the induction of apoptotic cell death. Untreated PC-3 cells show high DNA binding activity of nuclear factor KB (NF-KB), an antiapoptotic transcriptional factor, but this was inhibited by SVT and accompanied by a significant inhibition of p50 translocation into the nucleus, as well as phosphorylation of inhibitory KB. Consistent with the induction of apoptosis and inhibition of NF-KB, this toxin increased the expression of proapoptotic proteins such as p53, Bax, caspase-3, and caspase-9, but down-regulated antiapoptotic protein Bcl-2. However, SVT did not show an inhibitory effect on cell growth and caspase-3 activity in cells carrying mutant p50 and inhibitory KB kinase plasmids. Confocal microscopy analysis showed that SVT is taken up into the nucleus of the cells. These findings suggest that a nanogram concentration range of SVT from V. lebetina turanica could inhibit hormone-refractory human prostate cancer cell growth, and the effect may be related to NF-KB signal -mediated induction of apoptosis. [Mol Cancer Ther 2007;6(2):675 -83]

show abstract

Section: Discussionmentioning

confidence: 99%

Inhibitory effect of snake venom toxin from Vipera lebetina turanica on hormone-refractory human prostate cancer cell growth: induction of apoptosis through inactivation of nuclear factor κB

Son¹,

Park²,

Chae

et al. 2007

Molecular Cancer Therapeutics

View full text Add to dashboard Cite

show abstract

“…33 Besides that, the presence of a disintegrin-like domain in P-III SVMPs may confer different properties to the metalloproteinases as blocking integrin signaling or inducing a direct signal transduction by interaction with integrin receptors. 36 It has been shown that classical RGD-disintegrins [37][38][39] induce apoptosis by interfering with α v β 3 attachment to ECM proteins. Isolated disintegrin-like domains of P-III SVMPs may also induce apoptosis as shown by You and coworkers using the recombinant disintegrin domain of halysase.…”

Section: Discussionmentioning

confidence: 99%

“…42 In addition, the binding of alternagin-C to endothelial cells initiates signaling cascades leading to the activation of PI3K-Akt/PKB survival pathway. Therefore, the main difference between jararhagin and other SVMPs could be related to an eventual anti-apoptotic effect of jararhagin disintegrin domain, as observed in cultures of endothelial cells under suspension, in spite of the apoptotic action induced by other disintegrins [37][38][39] or EDTA-inactivated SVMPs such as halysase. 26 The effects of jararhagin were also studied in cultures of fibroblasts and in murine peritoneal adherent cells (MPACs).…”

Section: Discussionmentioning

confidence: 99%

Jararhagin, a snake venom metalloproteinase, induces a specialized form of apoptosis (anoikis) selective to endothelial cells

Tanjoni

Weinlich²,

Della-Casa

et al. 2005

Apoptosis

View full text Add to dashboard Cite

Jararhagin is a snake venom metalloproteinase (SVMP) from Bothrops jararaca involved in several hemostatic and inflammatory disorders that occur in human envenomings. In this study, we evaluated the effect of jararhagin on endothelial cells (tEnd). The exposure of tEnd to jararhagin (20 and 40microg/ml) resulted in apoptosis with activation of pro-caspase-3 and alterations in the ratio between Bax/Bcl-xL. We observed that apoptosis was followed by decrease of cell viability and the loss of cell adhesion. Jararhagin induced changes in cell shape with a decrease in cell spreading, rounding up and detachment. This was accompanied by a rearrangement of actin network and a decrease in FAK association to actin and in tyrosine phosphorylated proteins. Morphological alterations and apoptosis were abolished when jararhagin catalytic activity was inhibited, indicating the importance of catalysis. Treatment of murine peritoneal adherent cells or fibroblasts with jararhagin did not result in apoptosis. The data indicate that the pro-apoptotic effect of jararhagin is selective to endothelial cells, interfering with the adhesion mechanisms and inducing anoikis. The present model might be useful for the study of the relationships between the architectural changes in the cytoskeleton and the complex phenomenon named anoikis.

show abstract

“…Investigations into this mechanism (Kauskot et al, 2008;Marcinkiewicz et al, 1997) showed that the interaction of the RGD disintegrins with α IIb β 3 integrin block the connection with fibrinogen, thereby This binding also contributes to the appearance of bleeding (Hong et al, 2003).…”

Section: Disintegrinsmentioning

confidence: 99%

The role of platelets in hemostasis and the effects of snake venom toxins on platelet function

Queiroz

Sousa

Pereira

et al. 2017

Toxicon

View full text Add to dashboard Cite

The snake venom disintegrin salmosin induces apoptosis by disassembly of focal adhesions in bovine capillary endothelial cells

Cited by 44 publications

References 27 publications

Inhibitory effect of snake venom toxin from Vipera lebetina turanica on hormone-refractory human prostate cancer cell growth: induction of apoptosis through inactivation of nuclear factor κB

Inhibitory effect of snake venom toxin from Vipera lebetina turanica on hormone-refractory human prostate cancer cell growth: induction of apoptosis through inactivation of nuclear factor κB

Jararhagin, a snake venom metalloproteinase, induces a specialized form of apoptosis (anoikis) selective to endothelial cells

The role of platelets in hemostasis and the effects of snake venom toxins on platelet function

Contact Info

Product

Resources

About