Upregulation of GADD45α by Lentivirus vector enhances the drugsensitivity of imatinib-resistant K562IR cells

Acta Universitatis Medicinalis Anhui 2021 12 v.56 1920-1924     font:big middle small

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Authors:Liu Xueni;Wang Chao;Cheng Yanhong; Yang Peng

Keywords:chronic myeloid leukemia;K562;GADD45α;imatinib;drug resistance

DOI:10.19405/j.cnki.issn1000-1492.2021.12.014

〔Abstract〕 Objective To investigate the effects of up-regulation of GADD45α by Lentivirus vector on the proliferation, migration and apoptosis of imatinib-resistant K562 IR cells. Methods K562 cells and imatinib-resistant K562 IR cells were cultured. The expression levels of GADD45α mRNA and protein in K562 and K562 IR cells were detected by qRT-PCR and Western blot. The Lentivirus vector that over-expressed GADD45α and control were transfected in K562 IR cells, respectively Lv-GADD45α and Lv-NC. The expression level of GADD45α in each group was detected by Western blot, and the changes in cell proliferation, migration and apoptosis after transfection were further detected by CCK-8, Tanswell and Annexin V-FITC/PI double staining. Results The expression levels of GADD45α protein and mRNA in K562 IR cells were lower than those in K562 cells. After GADD45α was transfected, the expression levels of GADD45α in Lv-GADD45α group were higher than those in Lv-NC group. After imatinib treatment, the IC50value of Lv-GADD45α group was lower than that of Lv-NC group, the apoptosis rate of cells in Lv-GADD45α group was higher than that of the Lv-NC group, and the cell migration ability also decreased, with statistically significant difference(P<0.05). Conclusion By up-regulating GADD45α in imatinib-resistant K562 IR cells, the sensitivity of K562 IR to imatinib in chronic myeloid leukemia cells is enhanced, leading to proliferation inhibition and the apoptosis of chronic myeloid leukemia cells.