Arsenic trioxide downregulates cancer procoagulant activity in MCF-7 and WM-115 cell lines in vitro

Hoffman, Ewelina; Gizelska, Katarzyna; Mirowski, Marek; Mielicki, Wojciech P.

doi:10.5114/wo.2014.41390

Cited by 10 publications

(10 citation statements)

References 33 publications

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“…Previous studies show that chemotherapeutic agents increase cancer PCA that will be downregulated by differentiation drugs like arsenic trioxide and is closely associated with PS exposure. 25,26 In this study, platelets after chemotherapy or treated with cisplatin in vitro have significantly elevated PS exposure, and some platelets are even apoptotic. Blockade of PS with lactadherin on platelets inhibits thrombin and fibrin formation by approximately 70%.…”

Section: Discussionmentioning

confidence: 56%

Enhanced procoagulant activity of platelets after chemotherapy in non-small cell lung cancer

Kou

et al. 2017

Cancer Biology & Therapy

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The procoagulant status of patients with non-small cell lung cancer (NSCLC) after chemotherapy is poorly characterized and the role of platelets in hypercoagulative state of NSCLC is unknown. The aim of this study was to evaluate the procoagulant activity (PCA) of platelets in NSCLC before and after chemotherapy. The subjects were 52 patients newly diagnosed with NSCLC. The patients had decreased clotting time compared with healthy subjects, and the thrombin-antithrombin complex increased 2.5-fold after chemotherapy. Platelets in the patients after chemotherapy had enhanced phosphatidylserine (PS) exposure, and shortened coagulation time as well as increased thrombin and fibrin formation of platelets compared with those before chemotherapy. Platelet-derived microparticles increased 2-fold at day 1 and peaked at day 2 post-chemotherapy. Treatment of cisplatin in vitro also resulted in upregulated intrinsic FXa and thrombin formation on platelets with a dose-dependent manner. Platelets treated with aspirin significantly decreased PCA. However, lactadherin blocked PS and inhibited the PCA approximately by 70%. Seven days after chemotherapy, PCA of platelets restored to the baseline as that before chemotherapy, indicating that within a week of chemotherapy patient platelets are highly procoagulant and effective intervention should be taken in case of thrombosis. Our results suggested that platelets after chemotherapy had elevated PCA and may contribute to the hypercoagulative state of NSCLC. Prophylactic anti-coagulant combined with anti-platelet therapy may play an inhibitory role in thrombotic complications in NSCLC.

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Section: Discussionmentioning

confidence: 56%

Enhanced procoagulant activity of platelets after chemotherapy in non-small cell lung cancer

Kou

et al. 2017

Cancer Biology & Therapy

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“…Experimental results using New Zealand rabbits as animal models (11) indicated that no significant difference existed between 40 µg As 2 O 3 DES and 180 µg paclitaxel DES in reducing intimal hyperplasia. Experimental results using pigs as an animal model (14) demonstrated that AVI can reduce intimal proliferation following coronary artery damage without significantly delaying the vascular endothelial process at the stent implantation site and has a significant effect on restenosis rates.…”

Section: Discussionmentioning

confidence: 98%

“…It has been demonstrated that stents coated with anticancer drugs may significantly inhibit the proliferation of smooth muscle cells following PCI and reduce the restenosis rate (5). A number of studies have demonstrated that, as an anti-cancer agent, arsenic trioxide (As 2 O 3 ) is able to treat leukemia and other malignant tumors by inducing the apoptosis of tumor cells (6)(7)(8)(9)(10)(11)(12). The mechanism by which arsenic trioxide prevents restenosis is through attenuating smooth muscle cell proliferation by inhibiting the G1 and S phases of the cell cycle, as well as promoting apoptosis (13)(14)(15).…”

Section: Introductionmentioning

confidence: 99%

Efficacy of arsenic trioxide drug-eluting stents in the treatment of coronary heart disease

Zhang

et al. 2017

Experimental and Therapeutic Medicine

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Abstract. The aim of the current study was to evaluate the safety and clinical efficacy of arsenic trioxide drug-eluting (AVI) stents, manufactured in China, for the treatment of coronary heart disease (CHD). Between January and August 2014, 40 patients with CHD admitted to Yongchuan Hospital with implanted AVI stents alone were selected. A one-year clinical follow-up was completed and one year postoperative coronary angiography was reviewed. Major adverse cardiovascular events (MACE), recurrent angina, stent restenosis and stent thrombosis cases were detected. All 40 patients with CHD completed the one-year clinical follow-up, as well as the one-year postoperative coronary angiography. The follow-up results indicated that the MACE rate was 15.0% (6/40), the target lesion revascularization rate was 15.0% (6/40), the angina recurrence rate was 32.5% (13/40), the in-stent restenosis rate was 20.0% (8/40) and the stent thrombosis rate was zero. There were no cases of cardiac death or nonfatal myocardial infarction. The incidence of restenosis was higher following implantation of the AVI stent and the safety and clinical efficacy were worse than expected.

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“…To achieve a response in malignant tumors, several organic arsenics have been designed for anticancer therapy [11]. Their anticancer mechanisms are different from those of ATO, including actions on tumor angiogenesis and metabolism as well as cell signaling pathways [12][13][14]. A compound called 2,3dimercaptopropanol, better known as British anti-Lewisite (BAL; dimercaprol) was synthesized by biochemists at Oxford University approximately one century ago and is still stored currently in hospital pharmacies and is occasionally employed in emergencies [15].…”

Section: Introductionmentioning

confidence: 99%

A formula constituted by arsenic trioxide and dimercaprol enhances sensitivity of pancreatic cancer xenografts to radiotherapy

Han¹,

Wu²,

Liu³

et al. 2020

Preprint

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Objective To investigate the efficacy of the formula constituted by arsenic trioxide (ATO) and dimercaprol (BAL), BAL-ATO, as a radiosensitizer against pancreatic cancer xenografts. Methods Four treatment arms, including the control, radiotherapy (RT), BAL-ATO and RT + BAL-ATO, were examined using mouse models bearing SW 1990 human pancreatic cancer xenografts. Besides survival and tumor volume analysis, living imaging for cell apoptosis in tumor samples, confocal laser microscope observation for hypoxia, western blot and immunohistochemistry (IHC) assays were employed to detect the mechanism of BAL-ATO in radiotherapy. Results The median survival of the combination (RT + BAL-ATO) group (64.5 days) was significantly longer than those of the control (49.5 days), RT (39 days), and BAL-ATO (48 days) groups ( P < 0.001 ). Compared to the control group, RT + BAL-ATO inhibited the growth of tumors in mice by 73%, which was much higher than the rate of inhibition of RT alone (59%). The further analysis results also showed an improved microenvironment with regard to hypoxia in tumors treated by BAL-ATO alone or RT + BAL-ATO; besides, the suppression of signals, such as CD24, CD44, ALDH1A1, Gli-1 and Nestin, those associating with pancreatic cancer stem cells (PCSCs), were detected in the tumor samples treated by BAL-ATO alone or RT combing with BAL-ATO. Conclusion The data suggested that BAL-ATO, a formula constituted by ATO and BAL, could function as a sensitizer to radiotherapy for pancreatic cancer xenografts, and the mechanism might be attributed to hypoxia reduction and inhibition to signal pathways associated with PCSCs.

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Arsenic trioxide downregulates cancer procoagulant activity in MCF-7 and WM-115 cell lines in vitro

Cited by 10 publications

References 33 publications

Enhanced procoagulant activity of platelets after chemotherapy in non-small cell lung cancer

Enhanced procoagulant activity of platelets after chemotherapy in non-small cell lung cancer

Efficacy of arsenic trioxide drug-eluting stents in the treatment of coronary heart disease

A formula constituted by arsenic trioxide and dimercaprol enhances sensitivity of pancreatic cancer xenografts to radiotherapy

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