The Establishment Of Contact And Adhesion Drug Resistance Model In Leukemia And The Preliminary Study Of Its Mechanism

[Objective] Collect bone marrow specimens to detect the expression of Fn. Then partly simulate the ALL bone marrow microenvironment to demonstrate drug sensitivity changes of acute lymphoid leukemia cell line Jurkat to pirarubicin, when Jurkat cells exposed to bone marrow stramal cells(MSCs) and fibronectin(Fn).And discuss drug resistance in acute leukemia mediated by bone marrow microenvironment and certain mechanism.[Methods] collect some bone marrow specimens of different patients, detect the expression of Fn in bone marrow samples; use the CCK-8method to detecte the drug sensitivity of singly cultured Jurkat cells to pirarubicin in vitro; establish a co-culture model of Jurkat cells and bone marrow stromal cells(MSCs)/fibronectin(Fn) in vitro; use CCK-8and flow cytometry to detect changes of Jurkat cell apoptosis, then analyse the drug sensitivity changes of pirarubicin at the same concentration; use ELISA to detect the differences of Fn expression of level Jurkat cells in MSCs co-culture model compared with single cultured Jurkat cells model at different concentration of pirarubicin; using flow cytometry to demonstrate changes of the cycle arrest of Jurkat cells in the MSCs and Fn co-culture model compared with single cultured Jurkat cells model.[results] compared to samples of normal persons, patients with haemal tumor diseases demonstrated significantly high expression of Fn, the results were statistically significant; detections of ELISA in MSCs co-culture model showed expression of Fn in bone marrow stromal cells; In MSCs/Fn co-culture model, cell apoptosis changed obviously compared to single Jurkat cells cultured model at the same concentration of pirarubicin at the same time, with statistical significance; there were statistical significance of cell cycle arrest induced by MSCs/Fn co-culture model compared to single Jurkat cells model at the same concentration of pirarubicin at the same time.[Conclusion]bone marrow of patients with haemal tumor diseases can secrete higher levels of Fn compared with nomal persons; bone marrow stromal cells can secrete Fn MSCs, and probobly induce cell apoptosis, and G1cycle arrest in this way.