Song Ning, Wang Baohua, Feng Guishan, Duan Lin, Yuan Shengfang, Jia Weihua, Liu Yi
Department of Infectious Diseases, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei 050000, P.R. China.
Department of Thoracic Surgery, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei 050000, P.R. China.
Oncol Lett. 2019 Mar;17(3):2937-2945. doi: 10.3892/ol.2019.9927. Epub 2019 Jan 14.
Previous research has linked high mobility group box 3 (HMGB3) overexpression to the malignant progression and poor prognosis of non-small cell lung cancer (NSCLC). The present study investigated the role of HMGB3 in cell survival and colony formation of NSCLC cells. Stable knockdown of HMGB3 in A549 cells was achieved by lentiviral-based shRNA interference and verified by detection of the transcriptional and translational level of HMGB3 with reverse transcription-quantitative polymerase chain reaction and western blotting, respectively. The influence of HMGB3 knockdown on A549 cell viability and apoptotic rate was evaluated by Cell Counting Kit-8 assay and flow cytometry following annexin V staining, respectively. The proliferative capacity of A549 cells with or without HMGB3 knockdown was compared by measuring their colony forming efficiency. The results of the current study revealed that HMGB3 knockdown significantly reduced cell viability and colony forming efficiency while promoting apoptosis in A549 cells, indicating that HMGB3 may be pivotal for the survival and colony formation of A549 cells, serving a notable role in NSCLC progression.
先前的研究已将高迁移率族蛋白盒3(HMGB3)的过表达与非小细胞肺癌(NSCLC)的恶性进展及不良预后联系起来。本研究调查了HMGB3在NSCLC细胞存活和集落形成中的作用。通过基于慢病毒的短发夹RNA(shRNA)干扰实现了A549细胞中HMGB3的稳定敲低,并分别通过逆转录-定量聚合酶链反应和蛋白质印迹法检测HMGB3的转录和翻译水平进行了验证。分别通过细胞计数试剂盒-8法和膜联蛋白V染色后的流式细胞术评估了HMGB3敲低对A549细胞活力和凋亡率的影响。通过测量其集落形成效率比较了有或没有HMGB3敲低的A549细胞的增殖能力。当前研究结果显示,HMGB3敲低显著降低了A549细胞的活力和集落形成效率,同时促进了A549细胞的凋亡,表明HMGB3可能对A549细胞的存活和集落形成至关重要,在NSCLC进展中起显著作用。