Likewise, in case of Bax, the lec-pac-MNPs showed 5 fold higher increase in the expression. For the CML specific Bcr-Abl gene, the quantitative PCR results showed that the fold decrease in the expression in case of lec-pac-MNPs and pac-MNPs treated cells were 29 and 17 fold respectively whereas that of native pac was 2.4 fold compared to untreated cells. Also, there was decreased level of antiapoptotic signal proteins like Bcl-2 and the decrease was most significant in case of lec-pac-MNPs i.e, 42.4 fold. Finally, the quantitative PCR, revealed 16 fold increase in the level of cleaved caspase 3 in case of lec-pac-MNPs and 8 and 1.3 folds increase respectively in case of pac-MNPs and native pac as compared to control cells. At present most of the therapeutic modes for CML, includes chemotherapy, interferon mediated immunotherapy and bone marrow transplantation. The primary cause of treatment failures in leukemia is due to the resistance of leukemic cells to chemotherapy-induced apoptosis and emergence of MDR. The Bcr-Abl gene in CML activates the signaling pathways like PI3K/ AKT, Ras etc that confer growth CHIR-99021 GSK-3 inhibitor factor independent proliferation. In addition, CML cells are resistant to induction of apoptosis by variety of agents, such as TNFa, CD95/FasL etc.. Although, the advent of the abl tyrosine kinase inhibitor, imatinib, has revolutionized the treatment of CML, approximately 30% of CML patients develop intolerance to imatinib either due to point mutation or gene amplification. Activation of Srckinases, also EX 527 contribute to resistance in some cases. To reverse the resistance mechanism and to reduce the side effects of drugs, a promising approach is to combine the conventional chemotherapy with applications of nanotechnology. Palama et al. have used microcapsules for encapsulating imatinib drug and achieved increased drug retention and antitumor activity in CML stem cells and also improved the ex vivo purging of malignant progenitors from patient autografts. The up-regulated P-glycoprotein that increases the drug-efflux is considered as the key event for establishment of MDR in cancer cells and to counteract this, P-gp blockers and targeted drug deliverers are the major approaches. The targeted nanoparticles have attracted much attention due to their active targeting property. Selective expression of a cell surface antigen on target cells provides an opportunity for the antibody based therapy for both leukemia and solid tumors. C-type lectin molecules are identified as potential receptors expressed on normal myeloid and leukemic blast cells. Our results also demonstrated about five fold increase in the uptake efficiency after conjugation of lectin glycoprotein to the nanocarriers. This higher uptake of lec-pac- MNPs helped in delivering appropriate therapeutic concentration of paclitaxel to the K562 cells and in turn induced the cytotoxicity effect leading to apoptosis.