Ma Kun-Peng, Sun Zhen-Jiang, Shen Ying, Wang Yi-Qiang, Lin Dan-Dan
The First Affiliated Hospital of Soochow University, Jiangsu Institute of Hematology, Medical College, Soochow University, Suzhou 215000, Jiangsu Province, China.
The First Affiliated Hospital of Soochow University, Jiangsu Institute of Hematology, Medical College, Soochow University, Suzhou 215000, Jiangsu Province, China.E-mail:
Zhongguo Shi Yan Xue Ye Xue Za Zhi. 2023 Feb;31(1):50-56. doi: 10.19746/j.cnki.issn.1009-2137.2023.01.008.
To discover the relationship between matrix remodeling associated 7 () and acute B lymphoblastic leukemia (B-ALL), and explore the effect of on the biological functions of B-ALL cell line REH.
The expression of in blood diseases was searched and analyzed through BloodSpot database. Real-time qPCR was used to detect the expression level of in B-ALL cell line 697 and REH cells. Lentivirus-mediated shRNA interference technology was utilized to knock down the expression of in REH cells. The effects of on the biological functions of REH cells were studied by in vitro experiments. Cell proliferation was detected by CCK-8 assay, cell cycle was detected by PI staining, cell apoptosis was detected by Annexin V and 7-AAD staining, and the expression of apoptosis pathway related proteins was detected by Western blot.
Database analysis showed that was highly expressed in B-ALL patients, and real-time qPCR results showed that was also highly expressed in cell lines 697 and REH cells. Knockdown of in REH cells inhibited the cell proliferation and increased the percentage of G/G phase cells. After treatment with cytarabine, the apoptotic ratio was increased in -impaired REH cells, and the activation of caspase-3 and caspase-9 were also increased.
Knockdown of can reduce the malignancy of REH cells by inhibiting the cell proliferation and increasing the sensitivity of REH cells to cytarabine. These results indicate may be as a novel target for the treatment of B-ALL, and the potential usefulness of in B-ALL deserves further investigation.
探讨基质重塑相关蛋白7（）与急性B淋巴细胞白血病（B-ALL）的关系，并研究其对B-ALL细胞系REH生物学功能的影响。
通过BloodSpot数据库检索并分析在血液疾病中的表达情况。采用实时定量聚合酶链反应（qPCR）检测B-ALL细胞系697和REH细胞中 的表达水平。利用慢病毒介导的短发夹RNA（shRNA）干扰技术敲低REH细胞中 的表达。通过体外实验研究 对REH细胞生物学功能的影响。采用细胞计数试剂盒-8（CCK-8）法检测细胞增殖，碘化丙啶（PI）染色检测细胞周期，膜联蛋白V和7-氨基放线菌素D（7-AAD）染色检测细胞凋亡，蛋白质免疫印迹法检测凋亡相关蛋白的表达。
数据库分析显示， 在B-ALL患者中高表达，qPCR结果显示， 在细胞系697和REH细胞中也高表达。敲低REH细胞中 的表达可抑制细胞增殖，并增加G/G期细胞百分比。阿糖胞苷处理后， 表达降低的REH细胞凋亡率增加，半胱天冬酶-3（caspase-3）和半胱天冬酶-9（caspase-9）的激活也增加。
敲低 可通过抑制细胞增殖和增加REH细胞对阿糖胞苷的敏感性来降低REH细胞的恶性程度。这些结果表明， 可能是治疗B-ALL的新靶点，其在B-ALL中的潜在应用价值值得进一步研究。
