Effect of heparin on apoptosis in human nasopharyngeal carcinoma CNE2 cells

Li, Hong Liang; Ye, Kai He; Zhang, Hai Wei; Luo, Ying; Ren, Xian Da; Xiong, Ai Hua; Situ, Rui

doi:10.1038/sj.cr.7290101

Cited by 35 publications

(26 citation statements)

References 25 publications

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“…Heparins might directly bind to selectins, cell adhesion molecules whose expression is increased on tumour cells and that are postulated to promote tumour invasion 96,98 . Finally, heparins have been shown to mediate signalling by direct binding to the surface of a variety of cancer cells in vitro, attenuating cellular proliferation 99,100 .…”

Section: Anticoagulants As Anticancer Therapymentioning

confidence: 99%

Cancer and Venous Thromboembolic Disease: From Molecular Mechanisms to Clinical Management

et al. 2014

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bleeding, and disseminated intravascular coagulation 2 . Prevention and management of those complications in cancer patients can significantly affect patient treatment, prognosis, and quality of life.Venous thromboembolism (vte), which includes deep venous thrombosis (dvt) and pulmonary embolism, might precede or coincide with a diagnosis of cancer. In this patient group, vte can potentially complicate surgery, hospitalization, or systemic chemotherapy 3-5 . Risk for vte is increased by a factor of approximately 6 in patients with cancer compared with non-cancer patients, and patients with cancer account for 20% of all newly diagnosed cases of vte 6 . Postmortem studies suggest that the incidence of vte in cancer patients might be as high as 50%, in keeping with the finding that, after cancer itself, vte represents the second leading cause of death in hospitalized patients with cancer 7-9 .Venous thromboembolism is associated with high morbidity, mortality, and economic burden. Its diagnosis and management can interrupt essential cancer therapy and cause potentially serious bleeding complications 10 . Moreover, approximately 25% of cancer patients with vte require readmission because of bleeding or recurrent vte 11,12 . MECHANISMS UNDERLYING THE CANCER-ASSOCIATED PROTHROMBOTIC PHENOTYPEDirect and indirect mechanisms contribute to the pathogenesis of cancer-associated vte 13-15 (Figure 1

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Section: Anticoagulants As Anticancer Therapymentioning

confidence: 99%

Cancer and Venous Thromboembolic Disease: From Molecular Mechanisms to Clinical Management

et al. 2014

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“…Thus, they may contribute to the natural processes of the body for the elimination of tumor cells. Heparin has an apoptotic effect on human hepatoma cells [22] , human nasopharyngeal carcinoma cells [23] and peripheral blood neutrophils [24] , possibly by interfering with transcription factor function [25] . Derivatives of heparin and chondroitin sulfate induce apoptosis of myeloma and breast cancer cells in vitro [26] .…”

Section: Gags and Apoptosismentioning

confidence: 99%

Neuroprotective Properties of Glycosaminoglycans: Potential Treatment for Neurodegenerative Disorders

et al. 2008

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Previous studies suggest that proteoglycans and glycosaminoglycans (GAGs) may play an important role in the pathogenesis and/or alleviation of neurodegenerative disorders, including Alzheimer’s disease (AD). Proteoglycans increase the formation of neurofibrillary tangles, and stimulate the aggregation of β-amyloid (Aβ). This effect, on the other hand, is believed to be competitively inhibited by certain GAGs. Over the past few years, we have examined the neuroprotective properties of Neuroparin (C3), a low-molecular-weight GAG (approx. 2.1 kDa), in animal models of lesions characteristic of AD. Neuroparin is composed of 4–10 oligosaccharides, and it is derived from heparin involving depolymerization of heparin by gamma irradiation. In our experiments, Neuroparin protected against cholinergic lesions induced by intracerebroventricular injection of a specific cholinotoxin, AF64A, in rats. Administration of Neuroparin attenuated AF64A-stimulated, low-affinity nerve growth factor receptor-immunoreactive axonal varicosities in the rat septum, and increased arborization of hippocampal CA1 neurons. Neuroparin also reduced the septal caspase 3 immunoreactivity induced by AF64A treatment. Moreover, Neuroparin reduced tau 2 immunoreactivity in the rat hippocampus, stimulated by intra-amygdaloid injection of Aβ_25–35. These findings are in good agreement with our previous data indicating a neuroprotective role of GAGs. These results, plus others, all suggest that Neuroparin may possess neuroprotective properties against many of the characteristic neural lesions in AD. Since our pharmacokinetic studies revealed that Neuroparin is capable of crossing the blood-brain barrier, Neuroparin may, conceivably, open an entirely new avenue in the treatment of neurodegenerative disorders. Phase I studies have been completed, and have proven to be extremely supportive in that regard.

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“…Diverse effects of heparin on malignant process are mostly based on its inhibition of angiogenic factors, such as bFGF, or interference of metastatic process containing heparanase or selectin mediated cell invasion, and to a lesser extent, on the activity to impede tumor growth and possibly carcinogenesis itself. In addition, several other observations for the apoptotic activities of heparin have been reported (5,6). For example, heparin inhibits activator protein-1, which is the nuclear target of many oncogenic signal transduction pathways (7), and it may bind with DNA through charge to charge interaction; in turn, transcription factors can be upregulated in both the cytosol and the nucleus (8).…”

Section: Introductionmentioning

confidence: 99%

Antiangiogenic and Apoptotic Properties of a Novel Amphiphilic Folate-Heparin-Lithocholate Derivative Having Cellular Internality for Cancer Therapy

Lee

Kim

et al. 2007

Pharm Res

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Purpose. Anitangiogenic and apoptotic properties of a novel chemically modified heparin derivative with low anticoagulant activity were evaluated on the experimental in vitro and in vivo model. Materials and Methods. Heparin-lithocholate conjugate (HL) was initially synthesized by covalently bonding lithocholate to heparin. Folate-HL conjugate (FHL) was further synthesized by conjugating folate to HL. Antiangiogenic and apoptotic abilities of HL and FHL were characterized in vitro and in vivo experimentations. Results. Compared to unmodified heparin, both HL and FHL represented a low anticoagulant activity (38 and 28%, respectively). HL and FHL maintained antiangiogenic activity even further modification from the results of Matrigel plugs assay. FHL specifically induced apoptosis on KB cells having highly expressed folate receptor after cellular internalization. Both administered HL and FHL had similar antiangiogenic activity and inhibitory effect on tumor growth in vivo although FHL induced higher apoptosis on tumor tissues. Conclusions. In vivo tumor growth inhibition was possibly due to the decrease of vessel density and apoptotic cell death, although antiangiogenic effect of FHL seemed more actively affected on growth inhibition than apoptotic potential in vivo system. Thus, Low anticoagulant FHL having antiangiogenic and apoptotic properties would provide benefits for the development of a new class of anticancer agent.

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Effect of heparin on apoptosis in human nasopharyngeal carcinoma CNE2 cells

Cited by 35 publications

References 25 publications

Cancer and Venous Thromboembolic Disease: From Molecular Mechanisms to Clinical Management

Cancer and Venous Thromboembolic Disease: From Molecular Mechanisms to Clinical Management

Neuroprotective Properties of Glycosaminoglycans: Potential Treatment for Neurodegenerative Disorders

Antiangiogenic and Apoptotic Properties of a Novel Amphiphilic Folate-Heparin-Lithocholate Derivative Having Cellular Internality for Cancer Therapy

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