Cisplatin Reduces Endothelial Cell Migration Via Regulation of Type 2-Matrix Metalloproteinase Activity

Montiel, Mercedes; Urso, Loredana; Esther, Blanca; Marsigliante, Santo; Jiménez, Eugenio

doi:10.1159/000218191

Cited by 33 publications

(25 citation statements)

References 35 publications

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“…3B; Pb.05), compared to vehicle-treated cells. Since MMP-2 and MMP-9 are involved in HUVEC migration [22], we also examined the effect of piperine on MMP-2 and MMP-9 expression by HUVECs. Western blot analysis showed that 24-h treatment of HUVECs with 100 μM piperine did not affect MMP-2 or MMP-9 expression (data not shown).…”

Section: Piperine Attenuates Endothelial Cell Migrationmentioning

confidence: 99%

Piperine, a dietary phytochemical, inhibits angiogenesis

Doucette

Hilchie

Liwski

et al. 2013

The Journal of Nutritional Biochemistry

104

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Angiogenesis plays an important role in tumor progression. Piperine, a major alkaloid constituent of black pepper, has diverse physiological actions including killing of cancer cells; however, the effect of piperine on angiogenesis is not known. Here we show that piperine inhibited the proliferation and G(1)/S transition of human umbilical vein endothelial cells (HUVECs) without causing cell death. Piperine also inhibited HUVEC migration and tubule formation in vitro, as well as collagen-induced angiogenic activity by rat aorta explants and breast cancer cell-induced angiogenesis in chick embryos. Although piperine binds to and activates the cation channel transient receptor potential vanilloid 1 (TRPV1), its effects on endothelial cells did not involve TRPV1 since the antiproliferative effect of piperine was not affected by TRPV1-selective antagonists, nor did HUVECs express detectable TRPV1 mRNA. Importantly, piperine inhibited phosphorylation of Ser 473 and Thr 308 residues of Akt (protein kinase B), which is a key regulator of endothelial cell function and angiogenesis. Consistent with Akt inhibition as the basis of piperine's action on HUVECs, inhibition of the phosphoinositide-3 kinase/Akt signaling pathway with LY-294002 also inhibited HUVEC proliferation and collagen-induced angiogenesis. Taken together, these data support the further investigation of piperine as an angiogenesis inhibitor for use in cancer treatment.

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Section: Piperine Attenuates Endothelial Cell Migrationmentioning

confidence: 99%

Piperine, a dietary phytochemical, inhibits angiogenesis

Doucette

Hilchie

Liwski

et al. 2013

The Journal of Nutritional Biochemistry

104

View full text Add to dashboard Cite

show abstract

“…Han and Chesney recently demonstrated that forced overexpression of the taurine transporter TauT protects LLC-PK1 proximal tubular renal cells against cisplatininduced apoptosis in vitro and they suggested that functional TauT plays a critical role in protecting against cisplatin-induced nephrotoxicity, possibly by attenuation of a p53-dependent pathway [29]. Cisplatin is shown to increase p38 activity [37] and p38 is known to be upstream of activation of p53 [38]. It is thus possible that the effect of TauT could involve an inhibition of p38.…”

Section: Taurine and Taut In Cisplatin Resistancementioning

confidence: 99%

Pinpointing Differences in Cisplatin-induced Apoptosis in Adherent and Non-adherent Cancer Cells

Tastesen

Holm

Møller³

et al. 2010

Cell Physiol Biochem

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Platinum compounds are used in the treatment of cancer. We demonstrate that cisplatin-induced (10 µM) apoptosis (caspase-3 activity) is pronounced within 18 hours in non-adherent Ehrlich ascites tumour cells (EATC), whereas there is no increase in caspase-3 activity in the adherent Ehrlich LettrÉ ascites tumour cells (ELA). Loss of KCl and cell shrinkage are hallmarks in apoptosis and has been shown in EATC. However, we find no reduction in cell volume and only a minor loss of K⁺ which is accompanied by net uptake of Na⁺ following 18 hours cisplatin exposure in ELA. Glutathione and taurine have previously been demonstrated to protect cells from apoptosis. We find, however, that increase or decrease in the cellular content of glutathione and taurine has no effect on cisplatin-induced cell death in EATC and ELA. Nevertheless, knock-down of the taurine transporter TauT leads to a significant increase in apoptosis in ELA following cisplatin exposure. We find that cytosolic accumulation of cisplatin is similar in EATC and ELA. However, the nuclear accumulation and DNA-binding of cisplatin is significant lower in ELA compared to EATC. We suggest three putative reasons for the observed cisplatin insensitivity in the adherent tumor cells (ELA) compared to the non-adherent tumor cells (EATC): less nuclear cisplatin accumulation, increased TauT activity, and decreased anion and water loss.

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“…It has been suggested that damage to the arterial wall layers through proteolytic, oxidative, or autoimmune mechanisms in inflammatory or infective processes may lead to carotid artery dissection [10]. Cisplatin can directly injure the endothelium and also reduce endothelial cell migration, an essential process for vascular remodelling and regeneration in several physiological and pathological situations, potentially predisposing to dissection [11]. …”

Section: Discussionmentioning

confidence: 99%

Acute Stroke Secondary to Carotid Artery Dissection in a Patient with Germ Cell Tumour: Did Cisplatin Play a Role?

Khadjooi¹,

Kenton²

2013

Oncol Res Treat

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Background: Cisplatin-based chemotherapy – mainly the bleomycin, etoposide and cisplatin (BEP) regimen – has significantly improved the prognosis of testicular germ cell tumours (GCT). However, it has serious vascular side effects, including acute ischemic stroke. Case Report: A 37-year-old man with no conventional cerebrovascular risk factors presented with right arm clumsiness followed by a transient episode of expressive dysphasia 3 h later. He was receiving the third cycle of BEP for metastatic retroperitoneal GCT. Brain computed tomography (CT) and diffusion-weighted magnetic resonance imaging (MRI) confirmed multiple acute infarctions in the left middle cerebral artery territory. MR angiography and CT angiography showed a dissection with flaps extending into the left internal and external carotid arteries. The patient was anticoagulated and made an almost complete recovery. Conclusion: Carotid artery dissection has not been reported as the cause of cisplatin-associated stroke in patients with GCT. This case demonstrates the potential for cisplatin-induced mechanisms causing carotid dissection, particularly considering the close temporal association of BEP and the event in our patient. In young patients with excellent curative potential from GCT, every effort should be made to minimise the risk of disabling side effects of BEP. After a stroke, imaging of intracranial and extracranial arteries, monitoring and correction of serum magnesium is recommended. The decision to continue or discontinue cisplatin-based chemotherapy should be individualised.

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Cisplatin Reduces Endothelial Cell Migration Via Regulation of Type 2-Matrix Metalloproteinase Activity

Cited by 33 publications

References 35 publications

Piperine, a dietary phytochemical, inhibits angiogenesis

Piperine, a dietary phytochemical, inhibits angiogenesis

Pinpointing Differences in Cisplatin-induced Apoptosis in Adherent and Non-adherent Cancer Cells

Acute Stroke Secondary to Carotid Artery Dissection in a Patient with Germ Cell Tumour: Did Cisplatin Play a Role?

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