转染
细胞生长
分子生物学
细胞凋亡
活力测定
癌症研究
生物
报告基因
化学
细胞培养
基因表达
基因
生物化学
遗传学
作者
Renjie Chai,Chong Xu,Ling Lü,Xinwei Li,Zhuang Ma
标识
DOI:10.1080/08923973.2021.1966032
摘要
To determine the role of quercetin in non-small cell lung carcinoma (NSCLC) and the biological outcomes using transfection experiments.Real-time reverse transcription-PCR and data collection were performed to determine lncRNA and miRNA levels. Transwell assay was performed to assess the invasion ability of cells. Apoptosis of cells digested with trypsin was determined using the Annexin V-FITC kit. Luciferase activity was determined using the luciferase reporter gene system. Cell viability was tested using the Cell Counting Kit-8 assay. A xenograft mouse model was established to investigate the effects of quercetin on tumor growth.The expression levels of the long non-coding RNA (lncRNA) small nucleolar RNA host gene 7 (SNHG7) were elevated in NSCLC cells, and the expression levels of the microRNA miR-34a-5p were decreased compared with those in normal cells. Further investigation revealed that quercetin decreased SNHG7 and elevated miR-34a-5p levels in NSCLC cells (p < .05). The luciferase reporter gene assay, RNA-binding protein immunoprecipitation assay, and transfection experiments revealed target-binding sequences between SNHG7 and miR-34a-5p. Overexpression of SNHG7 or miR-34a-5p inhibitor promoted NSCLC cell proliferation and accelerated tumor cell growth and metastasis. The therapeutic effect of quercetin on NSCLC cells was counteracted by co-transfection of SNHG7 mimic or miR-34a-5p inhibitor. Quercetin inhibited the survival, proliferation, migration, and invasion of NSCLC cells and enhanced their apoptosis. Using the mouse model, quercetin was shown to inhibit tumor growth.Quercetin inhibits the proliferation and induces apoptosis of NSCLC cells by mediating signaling via the lncRNA SNHG7/miR-34a-5p pathway.
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