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目的:探讨硼替佐米提高耐药K562/ADM细胞对NK细胞杀伤敏感性的可能机制。方法:流式细胞术和real-time PCR检测硼替佐米处理前后K562/ADM细胞表面MHCⅠ类链相关分子A(major histocompatibility complex classⅠchain-related molecule A,MICA)蛋白和mRNA的表达,LDH释放法检测硼替佐米处理前后K562/ADM细胞对NK细胞的杀伤敏感性。结果:硼替佐米处理后,K562/ADM细胞表面MICA蛋白表达率上升[(17.03±4.94)%vs(23.77±5.26)%,P<0.05];处理后K562/ADM细胞MICA mRNA的表达水平是处理前的(2.03±0.33)倍。效靶比为10∶1、20∶1时,NK细胞对硼替佐米处理后的K562/ADM细胞的杀伤率上升[(23.22±3.03)%、(30.30±0.74)%vs(33.69±1.28)%、(41.40±1.97)%,P<0.05]。结论:硼替佐米提高耐药K562/ADM细胞对NK细胞杀伤的敏感性,其机制可能与硼替佐米上调K562/ADM细胞MICA表达有关。
Objective: To explore the possible mechanism of bortezomib enhancing the sensitivity of K562 / ADM cells to NK cell killing. Methods: Flow cytometry and real-time PCR were used to detect the protein and mRNA expression of MHC class I chain-related molecule A (MICA) on the surface of K562 / ADM cells treated with bortezomib. LDH release assay K562 / ADM cell killing NK cell sensitivity before and after bortezomib treatment. Results: After treated with bortezomib, the expression of MICA protein in K562 / ADM cells was increased by (17.03 ± 4.94)% vs (23.77 ± 5.26)%, P <0.05] Before treatment (2.03 ± 0.33) times. The killing ratio of NK cells to Bortezomib-treated K562 / ADM cells increased by (23.22 ± 3.03)%, (30.30 ± 0.74)% vs (33.69 ± 1.28) %, (41.40 ± 1.97)%, P <0.05]. CONCLUSION: Bortezomib increases the sensitivity of drug-resistant K562 / ADM cells to NK cell killing in a mechanism that may be related to the up-regulation of MICA expression in K562 / ADM cells by bortezomib.