BRYOSTATIN-1, FENRETINIDE AND 1α, 25 (OH)2D3 INDUCE GROWTH INHIBITION, APOPTOSIS AND DIFFERENTIATION IN T AND B CELL-DERIVED ACUTE LYMPHOBLASTIC LEUKEMIA CELL LINES (CCRF-CEM AND NALM-6)

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ARDEKANI ALI M.; SOLEYMANI FARD SHAHRZAD; JEDDI TEHRANI MAHMOOD; GHAHREMANZADE RAMIN

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Journal: Avicenna Journal of Medical Biotechnology Year:2011 | Volume:3 | Issue:4 (11) Page(s): 177-193

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Title

BRYOSTATIN-1, FENRETINIDE AND 1α, 25 (OH)2D3 INDUCE GROWTH INHIBITION, APOPTOSIS AND DIFFERENTIATION IN T AND B CELL-DERIVED ACUTE LYMPHOBLASTIC LEUKEMIA CELL LINES (CCRF-CEM AND NALM-6)

Author(s)

ARDEKANI ALI M. | SOLEYMANI FARD SHAHRZAD | JEDDI TEHRANI MAHMOOD | GHAHREMANZADE RAMIN | Issue Writer Certificate

Keywords

ACUTE LYMPHOBLASTIC LEUKEMIA

APOPTOSIS

CELL DIFFERENTIATION

FLOW CYTOMETRY

Abstract

In many acute leukemias, normal differentiation does not occur. However, in many cell lines derived from hematologic malignancies, differentiation or APOPTOSIS can be induced by variety of agents. Despite advances in the treatment of ACUTE LYMPHOBLASTIC LEUKEMIA (ALL), in most patients long-term survival rates remain unsatisfactory, especially in T-cell derived ALL. Thus we studied the anticancer effects of fenretinide, 1a, 25 (OH)2D3, and bryostatin-1 in CCRF-CEM (T-cell derived) and Nalm-6 (B-cell derived) ALL cell lines. Using MTT assays, both cell lines were shown to exhibit increased inhibition of proliferation at micro (fenretinide) and nanomolar (1a, 25 (OH)2D3, bryostatin-1) concentrations. These anti-cancer agents were shown to induce APOPTOSIS and activate caspase-3 pathway in both ALL cell lines. Furthermore, for the first time we are reporting consistent anti-proliferative and apoptotic effects of Bryostatin-1 in ALL T-cell derived cell line with the lowest ED50 (ranging 4.6-7.4 nM). To evaluate the differentiation induction by fenretinide, 1a, 25 (OH)2D3, and bryostatin-1 in ALL cell lines, we assayed for the expressions of CD19, CD38 markers on Nalm-6 and CD7 marker on CCRF-CEM cell line. The flow cytometric analysis showed a significant increase in expression of CD markers in response to anticancer drug treatments. To assay the effects of anti-cancer drugs on cell cycle distribution, cell cycle analysis using FLOW CYTOMETRY was employed. These anti-cancer drugs appear to affect the CCRFCEM and Nalm-6 cell cycles differently (Go/G1 and G2/M arrest, respectively).Overall results demonstrate that the anticancer agents used in this study are strong inhibitors of ALL cell proliferation and inducers of APOPTOSIS and differentiationin vitro. These findings may be quite helpful if these drugs are to be used for dif-ferentiation therapy of ALL patients in clinics in the future. Further studies are warranted to establish thein vivo effect of these drugs particularly in patients with T-cell derived ALL.

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APA: Copy

ARDEKANI, ALI M., SOLEYMANI FARD, SHAHRZAD, JEDDI TEHRANI, MAHMOOD, & GHAHREMANZADE, RAMIN. (2011). BRYOSTATIN-1, FENRETINIDE AND 1α, 25 (OH)₂D₃ INDUCE GROWTH INHIBITION, APOPTOSIS AND DIFFERENTIATION IN T AND B CELL-DERIVED ACUTE LYMPHOBLASTIC LEUKEMIA CELL LINES (CCRF-CEM AND NALM-6). AVICENNA JOURNAL OF MEDICAL BIOTECHNOLOGY (AJMB), 3(4 (11)), 177-193. SID. https://sid.ir/paper/313764/en

Vancouver: Copy

ARDEKANI ALI M., SOLEYMANI FARD SHAHRZAD, JEDDI TEHRANI MAHMOOD, GHAHREMANZADE RAMIN. BRYOSTATIN-1, FENRETINIDE AND 1α, 25 (OH)₂D₃ INDUCE GROWTH INHIBITION, APOPTOSIS AND DIFFERENTIATION IN T AND B CELL-DERIVED ACUTE LYMPHOBLASTIC LEUKEMIA CELL LINES (CCRF-CEM AND NALM-6). AVICENNA JOURNAL OF MEDICAL BIOTECHNOLOGY (AJMB)[Internet]. 2011;3(4 (11)):177-193. Available from: https://sid.ir/paper/313764/en

IEEE: Copy

ALI M. ARDEKANI, SHAHRZAD SOLEYMANI FARD, MAHMOOD JEDDI TEHRANI, and RAMIN GHAHREMANZADE, “BRYOSTATIN-1, FENRETINIDE AND 1α, 25 (OH)₂D₃ INDUCE GROWTH INHIBITION, APOPTOSIS AND DIFFERENTIATION IN T AND B CELL-DERIVED ACUTE LYMPHOBLASTIC LEUKEMIA CELL LINES (CCRF-CEM AND NALM-6),” AVICENNA JOURNAL OF MEDICAL BIOTECHNOLOGY (AJMB), vol. 3, no. 4 (11), pp. 177–193, 2011, [Online]. Available: https://sid.ir/paper/313764/en

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