期刊
CANCER BIOLOGY & THERAPY
卷 21, 期 9, 页码 806-814出版社
TAYLOR & FRANCIS INC
DOI: 10.1080/15384047.2020.1787757
关键词
SLCO4A1-AS1; miR-223-3p; IKK alpha; NSCLC; NF-kappa B signaling pathway
类别
Globally, lung cancer is known as a major cause of cancer-associated death and non-small-cell lung cancer (NSCLC) accounts for majority of all cases. Growing evidence has emerged that long non-coding RNAs (lncRNAs) act as vital regulatory molecules in various malignancies. Nevertheless, the function of SLCO4A1 antisense RNA 1(SLCO4A1-AS1) in NSCLC is vague. This study intended to investigate the biological role and probable regulatory mechanism of SLCO4A1-AS1 in NSCLC. qRT-PCR revealed that SLCO4A1-AS1 level was upregulated in NSCLC. Function assays manifested that silence of SLCO4A1-AS1 attenuated NSCLC cell proliferation, migration and invasion but promoted NSCLC cell apoptosis. Furthermore, we disclosed that SLCO4A1-AS1 activated NF-kappa B pathway in NSCLC, and that IKK alpha, an NF-kappa B pathway-related gene, possessed an enhanced level in NSCLC tissues and cells. Importantly, miR-223-3p bound with SLCO4A1-AS1 and IKK alpha. Further, SLCO4A1-AS1 competitively bound with miR-223-3p to increase IKK alpha expression, thereby activating NF-kappa B signaling pathway. In conclusion, SLCO4A1-AS1 drove NSCLC progression by activating NF-kappa B signaling pathway via sponging miR-223-3p to enhance IKK alpha expression. Thus, SLCO4A1-AS1 might be a promising biomarker for NSCLC treatment.
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