Abstract
Substantial researches indicated that long non-coding RNAs (lncRNAs) exerted profound effects on chemo-resistance in cancer treatment. Nonetheless, the role of NORAD in non-small-cell lung cancer (NSCLC) remains unclear. In the present study, we chose NSCLC cell lines H446 and A549 to explore the function of non-coding RNA activated damage (NORAD) in response to cisplatin (DDP) resistance of NSCLC. Experimental data manifested that NORAD was up-regulated in DDP-resistant NSCLC tissues and cells. NSCLC patients with high NORAD expression suffered a poor prognosis. NORAD knockdown resensitized H446/DDP and A549/DDP to DDP. Besides, NORAD acted as a molecular sponge of miR-129-1-3p. MiR-129-1-3p showed a low level of expression in DDP-resistant NSCLC tissues. Moreover, miR-129-1-3p overexpression impaired DDP resistance in H446/DDP and A549/DDP cells. SOX4 was the downstream target of miR-129-1-3p. Especially, SOX4 overexpression offset the effects of NORAD silence on H446/DDP and A549/DDP cells resistance to DDP. NORAD knockdown resensitized H446/DDP and A549/DDP to DDP in NSCLC via targeting miR-129-1-3p/SOX4 axis, offering a brand-new target for NSCLC chemo-resistance.
Highlights
Lung cancer is considered as one of the most malignant cancers with high death rates around the world
RT-qPCR results revealed that Non-coding RNA Activated Damage (NORAD) was overexpressed in H446 and A549 cell compared with normal human lung bronchial epithelial BEAS-2B cell
DDP resistance restricted the effectiveness of chemotherapy among Non-small cell lung cancer (NSCLC) patients [18]
Summary
Lung cancer is considered as one of the most malignant cancers with high death rates around the world. Non-small cell lung cancer (NSCLC) counts for around 85% of all cases [1]. Especially cisplatin (DDP), chemotherapy is a main treatment strategy for NSCLC after surgical resection [2]. Cisplatin resistance influences the desirable effects of DDP in clinical therapy, lead to high death rates of NSCLC. Non-coding RNA Activated Damage (NORAD) is a lncRNA induced by DNA damage. A previous study indicated that NORAD overexpression was associated with accelerating progression of colorectal cancer [10]. It was discovered as a tumor promoter in colorectal cancer [11]. Its detailed function in DDP resistance has not been elucidated in NSCLC cells
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