Résumé
Aim To investigate the effect of long non-coding RNA (LncRNA) HIT on the resistance of ima-tinib (IM) in SUP-B15 cell line of acute lymphoblastic leukemia (ALL) and the related mechanisms. Methods SUP-B15 cells were treated with concentration gradient IM and saline as IMR and control groups. The lentivirus transfected LncRNA HIT shRNAl # and 2# vector in IMR group cells to knock down the HIT expression as IMR shHITl # and 2# group cells. CCK-8 assay was used to detect IM half-inhibitory concentration ( ICjo ). Fluorescence quantitative PCR (qPCR) was applied to detect the expression levels of LncRNA HIT, QKI, 0ct4 and Sox2 mRNA. Western blot was employed to detect the expression levels of QKI, 0ct4 and Sox2 protein. Results Compared with those in control cells, there was significantly higher IM ICjq, higher expression of LncRNA HIT, 0ct4 and Sox2, and lower expression of QKI in groups of IMR, IMR shHITl# and 2# cells. Compared with those in IMR cells, there was significantly lower IM IC∗, lower expression of LncRNA HIT, 0ct4 and Sox2, and higher expression of QKI in groups of IMR shHITl# and 2# cells. The difference was statistically significant (P < 0. 05). Conclusions LncRNA HIT can increase the expression of Sox2 and 0ct4 via inhibiting the expression of QKI protein, and mediating the formation of IM resistance in ALL cells.
Résumé
AIM: To study the expression profile of QKI m RNA and protein in rat heart during pathological cardiac hypertrophy. ME THODS: A rat cardiac hypertrophy model was established using continuous norepinephrine (NE) perfusion. Real-time PCR and Western blotting were applied t o examine QKI mRNA and protein expression respectively in rat heart. RES ULTS: Both mRNA and protein of three QKI isoforms were detected in adult rat heart. QKI-5 mRNA and total QKI protein were remarkably decreased in NE-ind uced hypertrophic heart compared with those in control group (P