Abstract
To investigate the relationship between long non-coding RNA (LncRNA) PANTR1 and imatinib resistance in chronic myeloid leukemia cell line K562 and its mechanism. K562 control cells (Control) and K562 imatinib resistant cells (ImR) were cultured. Two siRNA vectors targeting PANTR1 and control vectors were transfected into K562-ImR cells by lentivirus as ImR-siPA#1, ImR-siPA#2 and ImR-siControl cells, respectively. Imatinib semi-inhibitory concentration (IC50) was detected by CCK-8 kit. The expression level of PANTR1, BCR/ABL, MDR, CD44 and CD133 mRNA were detected by fluorescence quantitative PCR（RT-qPCR）, and the expression level of BCR/ABL, MDR, CD44 and CD133 protein were detected by Western blot. Imatinib IC50 in ImR cells was significantly higher than that in control cells (P＜0.01), that of ImR-siPA#1 and ImR-siPA#2 cells were significantly lower than that in ImR-sicontrol cells (P＜0.01), but still significantly higher than that in control cells (P＜0.01). The mRNA expression level of PANTR1, BCR/ABL, MDR, CD44 and CD133 in ImR cells were significantly higher than those in control cells (P＜0.01). The mRNA expression level of PANTR1, MDR, CD44 and CD133 in ImR-siPA#1 and ImR-siPA#2 cells were significantly lower than those in ImR-siControl cells (P＜0.01), while the expression level of BCR/ABL mRNA was not significantly different (P＞0.05). The protein expression level of BCR/ABL, MDR, CD44 and CD133 in ImR cells were significantly higher than those in control cells, while the protein expression level of MDR, CD44 and CD133 in ImR-siPA#1 and ImR-siPA#2 were significantly lower than those in ImR-siControl cells. LncRNA PANTR1 can promote the expression of MDR and stem cell marker in chronic myeloid leukemia cell line K562, and mediate imatinib resistance.
Published Version
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