Key result
Both aspirin (p≤0.05) and the P2Y12 inhibitor 2MeSAMP (p≤0.01) significantly decreased platelet-induced invasion capacity of SK-OV-3 ovarian cancer cells, reverting invasion to levels comparable to cancer cells alone.
Why the study?
Do aspirin and P2Y12 inhibition reduce platelet-induced invasion in ovarian cancer cell lines?
Do aspirin and P2Y12 inhibition reduce platelet-induced invasion in ovarian cancer cell lines?
Aspirin and P2Y12 inhibition attenuate platelet-induced invasion in ovarian cancer cell lines, suggesting a potential therapeutic role in inhibiting metastasis.
Answers are grounded in this paper and cite their sources.
Platelets promote invasion and EMT in SK-OV-3 cells; antiplatelet agents attenuate this in vitro, leaving clinical translation open.
BACKGROUND: Platelet-cancer cell interactions play a key role in successful haematogenous metastasis. Disseminated malignancy is the leading cause of death among ovarian cancer patients. It is unknown why different ovarian cancers have different metastatic phenotypes. To investigate if platelet-cancer cell interactions play a role, we characterized the response of ovarian cancer cell lines to platelets both functionally and at a molecular level. METHODS: Cell lines 59 M and SK-OV-3 were used as in vitro model systems of metastatic ovarian cancer. Platelet cloaking of each cell line was quantified by flow cytometry. Matrigel invasion chamber assays were used to assess the invasive capacity of the cell lines. The induction of an EMT was assessed by morphology analysis and by gene expression analysis of a panel of 11 EMT markers using TaqMan RT-PCR. RESULTS: SK-OV-3 cells adhered to and activated more platelets than 59 M cells (p = 0.0333). Platelets significantly promoted the ability of only SK-OV-3 cells to invade (p ≤ 0.0001). Morphology and transcritpome analysis indicated that platelets induce an epithelial-to-mesenchymal transition phenotype in both cells lines, with a more exaggerated response in SK-OV-3 cells. Next, we investigated if antiplatelet agents could abrogate the platelet-induced aggressive phenotype in SK-OV-3 cells. Both aspirin (p ≤ 0.05) and 2-methylthioadenosine 5'-monophosphate triethylammonium salt hydrate (P2Y12 inhibitor; p ≤ 0.01) significantly decreased their invasion capacity, and effectively reverted invasion to levels comparable to SK-OV-3 cells alone. CONCLUSION: While there is increasing evidence for the cancer-protective effect of aspirin, this study suggests P2Y12 inhibition may also play a role. Understanding these complex interactions between platelets and cancer cells could ultimately allow the establishment of therapies tailored to inhibiting metastasis, thus significantly reducing cancer morbidity.
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Cooke et al. (2015) studied Ovarian cancer. Aspirin and 2MeSAMP (P2Y12 inhibitor) vs. Untreated platelets was evaluated on Cancer cell invasion capacity (p=≤0.05). Both aspirin (p≤0.05) and the P2Y12 inhibitor 2MeSAMP (p≤0.01) significantly decreased platelet-induced invasion capacity of SK-OV-3 ovarian cancer cells, reverting invasion to levels comparable to cancer cells alone.
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