[Relationship between PANTR1 and Imatinib Resistance of Chronic Myeloid Leukemia Cell Line K562 and Its Related Mechanisms].

Objective: To investigate the relationship between long non-coding RNA (LncRNA) PANTR1 and imatinib resistance in chronic myeloid leukemia cell line K562 and its mechanism.

Methods: 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 (IC) 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.

Results: Imatinib IC 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.

Conclusion: LncRNA PANTR1 can promote the expression of MDR and stem cell marker in chronic myeloid leukemia cell line K562, and mediate imatinib resistance.