 |
JOURNAL TOOLS |
| Opzioni di pubblicazione |
| eTOC |
| Per abbonarsi |
| Sottometti un articolo |
| Segnala alla tua biblioteca |
ARTICLE TOOLS |
| Publication history |
| Estratti |
| Permessi |
| Per citare questo articolo |
| Share |
I TUOI DATI
I TUOI ORDINI
CESTINO ACQUISTI
N. prodotti: 0
Totale ordine: € 0,00
COME ORDINARE
I TUOI ABBONAMENTI
I TUOI ARTICOLI
I TUOI EBOOK
COUPON
ACCESSIBILITÀ
Minerva Medica 2021 Mar 25
DOI: 10.23736/S0026-4806.21.07194-9
Copyright © 2021 EDIZIONI MINERVA MEDICA
lingua: Inglese
LncRNA NORAD accelerates the progression of non-small cell lung cancer via targeting miRNA-455/CDK14 axis
Chunyang WANG 1, Dongmei WU 2 ✉, Maofang HE 3, Li GUAN 3, Dan BAI 3, Baihui LIANG 1
1 College of Clinical Medicine, Xi’an Medical University, Xi’an, China; 2 Department of Radiation Oncology, Nanxishan Hospital of Guangxi Zhuang Autonomous Region, Guilin, China; 3 College of Pharmacy, Xi’an Medical University, Xi’an, China
BACKGROUND: To explore the potential involvement of long non-coding RNA (lncRNA) NORAD in regulating the progression of Non-small cell lung cancer (NSCLC), and its possible mechanism.
METHODS: Relative level of NORAD in NSCLC tissues and cell lines was determined. Its level in NSCLC patients with different tumor staging (T1-T2, T3-T4) and either with lymphatic metastasis or not was examined as well. Kaplan-Meier curves were depicted for assessing the prognostic value of NORAD in NSCLC. Regulatory effects of NORAD on the proliferative ability of NCI-H1650 and HCC827 cells were evaluated. Dual-luciferase reporter gene assay was conducted to identify the binding between NORAD and miRNA-455, as well as between miRNA-455 and CDK14. At last, the role of NORAD/miRNA-455/CDK14 regulatory loop in influencing the progression of NSCLC was determined.
RESULTS: NORAD was upregulated in NSCLC tissues and cells. Its level was higher in NSCLC patients with advanced stage or accompanied with lymphatic metastasis. Worse prognosis was observed in NSCLC patients presenting high level of NORAD. Silence of NORAD attenuated the proliferative ability of NCI-H1650 and HCC827 cells. MiRNA-455 was the downstream target binding to NORAD. Its level was negatively regulated by NORAD. Knockdown of miRNA-455 could reverse the role of NORAD in regulating the proliferative ability of NSCLC. Moreover, CDK14 was the target gene of miRNA-455. CDK14 level was negatively regulated by miRNA-455.
CONCLUSIONS: LncRNA NORAD is upregulated in NSCLC, which enhances the proliferative ability of tumor cells by targeting miRNA-455/CDK14 axis and thereby accelerates the progression of NSCLC.
KEY WORDS: Non-small cell lung cancer (NSCLC); NORAD; miRNA-455; CDK14; Proliferation