Treatment failure in T-cell acute lymphoblastic leukaemia (T-ALL) occurs when leukemic blasts acquire resistance to chemotherapeutic agents. Current research efforts are focused on the search for targets for the development of more effective and less toxic anti-leukemic drugs. CD47 has been suggested to be involved in chemo-resistance and cell metastasis. Although several potential mechanisms were suggested to explain the therapeutic effect of CD47-targeting; the downstream effectors which lead to different effects by CD47 are still not well understood. In this preliminary study we assessed the role of Protein kinase C (PKC) in CD47-mediated phosphatidylserine expression pathway in jurkat T cells. Jurkat T cells were incubated with anti-CD47 mAb (BRIC 126), anti-CD44 mAb (BRIC 235) or control in the presence or absence of Bisindolylmaleimide I, hydrochloride (PKC inhibitor). Cells were stained with annexin-V FITC. Flow cytometry analysis was used for measurement of fluorescence intensity. Cell viability was detected using trypan blue exclusion test. PKC inhibition enhanced phosphatidylserine expression in CD47 receptor mediated leukaemia cells apoptotic pathway. This indicates that PKC may be involved in CD47-mediated PS exposure pathway in jurkat T cells. The observations from this study identify CD47 and PKC as novel functional proteins in jurkat T cells with promising therapeutic potential. This study would provide insight for targeted therapy against T-ALL disease.
