A link between coagulation and clinical outcome of patients with cancer has been well established. Tissue factor (TF), a transmembrane glycoprotein known originally as the initiator of blood coagulation cascade, has recently been demonstrated to modify cancer microenvironment and angiogenesis. We have recently shown that anti-phospholipid antibody (aPL) mediate breast cancer tumor progression in xenograft model by up regulation of TF. We have further demonstrated that aPL stimulates TF expression in less aggressive tumor cell line (MDA-MB-468) but not aggressive cell line (MDA-MD-231), which expressed endogenously high level of TF. In our examination of the mechanism by which aPL stimulation leading to TF up regulation, we have discovered that microRNAs (miRs) play a significant role. Using the two cells with different endogenous expression of TF, we showed that miR106b is highly expressed in MDA-MB-468 compared to MDA-MB-231. Treatment of MDA-MB-468 with miR106b inhibitor released the inhibition of TF expression suggesting that miR106b negatively regulate TF expression. Our preliminary data show that aPL modifies miR106b expression in MDA-MB-468.

Antiphospholipid antibody and MiR106b mediated expression of tissue factor in breast cancer cell lines

252nd National Meeting (2016)

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