{"title":"Do Platelets Inhibit the Effect of Aspirin on Cancer Cells?","authors":"Neha Mehta, Sasikala Muthusamy, Alka Bhatia","doi":"10.1007/s12307-015-0169-7","DOIUrl":null,"url":null,"abstract":"<p><p>Both platelets and cancer cells display an intimate reciprocal crosstalk resulting in alteration of each other's properties. Although many past studies have tried to demonstrate effect of platelets on tumour cells, exact role of platelets in carcinogenesis is still not clear. In the above study, we explored the effect of different concentrations of platelet rich plasma (PRP) on viability, proliferation and adhesion of HeLa cells in culture conditions. The above parameters were found to be slightly increased on incubation with lower two concentrations of PRP (4.4 × 10(5) & 1 × 10(6) platelets/μl) while a reverse effect was seen at high PRP concentration (2 × 10(6) lac platelets/μl) especially at 24 h. To further validate that the above effects were due to platelets we repeated the experiments in the presence of antiplatelet drug aspirin (20 mM). On treatment with aspirin alone, the cell viability, proliferation and adhesion were seen to be decreased indicating cytotoxicity of aspirin towards HeLa cells. However, all of the above parameters were found to increase on addition of all PRP concentrations at 24 h. Overall, variations in the number of platelets produced different effects on the cancer cells. Use of aspirin reduced the viability of the cancer cells, but this effect was seen to be partially reversed by all the concentrations of PRP used. </p>","PeriodicalId":9425,"journal":{"name":"Cancer Microenvironment","volume":"8 2","pages":"119-22"},"PeriodicalIF":0.0000,"publicationDate":"2015-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s12307-015-0169-7","citationCount":"1","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cancer Microenvironment","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1007/s12307-015-0169-7","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2015/7/4 0:00:00","PubModel":"Epub","JCR":"Q2","JCRName":"Medicine","Score":null,"Total":0}
引用次数: 1
Abstract
Both platelets and cancer cells display an intimate reciprocal crosstalk resulting in alteration of each other's properties. Although many past studies have tried to demonstrate effect of platelets on tumour cells, exact role of platelets in carcinogenesis is still not clear. In the above study, we explored the effect of different concentrations of platelet rich plasma (PRP) on viability, proliferation and adhesion of HeLa cells in culture conditions. The above parameters were found to be slightly increased on incubation with lower two concentrations of PRP (4.4 × 10(5) & 1 × 10(6) platelets/μl) while a reverse effect was seen at high PRP concentration (2 × 10(6) lac platelets/μl) especially at 24 h. To further validate that the above effects were due to platelets we repeated the experiments in the presence of antiplatelet drug aspirin (20 mM). On treatment with aspirin alone, the cell viability, proliferation and adhesion were seen to be decreased indicating cytotoxicity of aspirin towards HeLa cells. However, all of the above parameters were found to increase on addition of all PRP concentrations at 24 h. Overall, variations in the number of platelets produced different effects on the cancer cells. Use of aspirin reduced the viability of the cancer cells, but this effect was seen to be partially reversed by all the concentrations of PRP used.
期刊介绍:
Cancer Microenvironment is the official journal of the International Cancer Microenvironment Society (ICMS). It publishes original studies in all aspects of basic, clinical and translational research devoted to the study of cancer microenvironment. It also features reports on clinical trials.
Coverage in Cancer Microenvironment includes: regulation of gene expression in the cancer microenvironment; innate and adaptive immunity in the cancer microenvironment, inflammation and cancer; tumor-associated stroma and extracellular matrix, tumor-endothelium interactions (angiogenesis, extravasation), cancer stem cells, the metastatic niche, targeting the tumor microenvironment: preclinical and clinical trials.