Long non‑coding RNA NORAD promotes cell proliferation and glycolysis in non‑small cell lung cancer by acting as a sponge for miR‑136‑5p

Gao, Wei; Weng, Ting; Wang, Lifang; Shi, Bin; Meng, Wenqi; Wang, Xiaoyu; Wu, Ying; Jin, Liang; Fei, Li-Juan

doi:10.3892/mmr.2019.10210

Cited by 29 publications

(26 citation statements)

References 29 publications

(30 reference statements)

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“…LncRNAs are reported to serve as ceRNAs to sponge miRNA, thus downregulating miRNA expressions [45]. For example, UCA1 upregulates the oncogene ERBB4 in lung cancer via binding to miR-193-3p [46]. LncRNA NORAD promotes cell proliferation and glycolysis in NSCLC by acting as a sponge for miR-136-5p [47].…”

Section: Discussionmentioning

confidence: 99%

LINC00922 Accelerates the Proliferation, Migration and Invasion of Lung Cancer Via the miRNA-204/CXCR4 Axis

Liang

Wang

et al. 2019

Med Sci Monit

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Background The aim of this study was to clarify the potential function of LINC00922 in regulating the progression of lung cancer and its underling mechanism. Material/Methods Relative levels of LINC00922 in lung cancer tissues and cell lines was determined by quantitative polymerase chain reaction. Correlation between LINC00922 levels and pathological indexes of lung cancer patients was analyzed through the chi-square test. Subsequently, regulatory effects of LINC00922 on the proliferative, migratory, and invasive capacities of PC9 and A549 cells were evaluated. Western blot was conducted to determine the role of LINC00922 in mediating protein levels of CXCR4, E-cadherin, and vimentin. Through dual-luciferase reporter gene assay and functional experiments, the potential function of LINC00922/miRNA-204/CXCR4 regulatory loop in mediating the progression of lung cancer was explored. Results LINC00922 was highly expressed in lung cancer and correlated to the poor prognosis of lung cancer patients. Overexpression of LINC00922 accelerated PC9 and A549 cells to proliferate, migrate, and invade. CXCR4 was upregulated in lung cancer tissues and cells, which promoted lung cancer cells to migrate and invade. LINC00922 regulated the level of CXCR4 and directly bound to miRNA-204/CXCR4. LINC00922 mediated the cellular behaviors of lung cancer cells via targeting the miRNA-204/CXCR4 axis. Conclusions LINC00922 was upregulated in lung cancer, and accelerated lung cancer cells to proliferate, migrate, and invade via targeting the miRNA-204/CXCR4 axis.

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Section: Discussionmentioning

confidence: 99%

LINC00922 Accelerates the Proliferation, Migration and Invasion of Lung Cancer Via the miRNA-204/CXCR4 Axis

Liang

Wang

et al. 2019

Med Sci Monit

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“…The outcomes exhibited that knockdown of NORAD dropped the cell viability and inhibited the proliferation in H446/DDP and A549/DDP cells ( Figure 1G,H). However, previous study has experimentally revealed that NORAD silencing dampen NSCLC cell proliferation [17]. It was probable that the negative impact on cell viability/proliferation was due to the interfering role of sh-NORAD on cell proliferation.…”

Section: Norad Was Overexpressed In Nsclc Tissues and Cellsmentioning

confidence: 94%

NORAD accelerates chemo-resistance of non-small-cell lung cancer via targeting at miR-129-1-3p/SOX4 axis

et al. 2020

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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.

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“…Both long non-coding RNA (lncRNA) and microRNA (miRNA) are common types of non-coding RNA (ncRNA) that have been studied extensively in recent decades ( He et al, 2018 ). The hypothesis that lncRNA can be used as “miRNA sponge” has been confirmed in many studies, which has become an essential way to elucidate the molecular mechanism of lncRNA ( Cui et al, 2017 ; Gao et al, 2019 ). Studies have shown that lncRNA has an important function in AS progression ( Xu et al, 2019 ).…”

Section: Introductionmentioning

confidence: 90%

“…The hypothesis that lncRNA can be used as "miRNA sponge" has been confirmed in many studies, which has become an essential way to elucidate the molecular mechanism of lncRNA (Cui et al, 2017;Gao et al, 2019). Studies have shown that lncRNA has an important function in AS progression (Xu et al, 2019).…”

Section: Introductionmentioning

confidence: 91%

lncRNA MEG3 Suppresses the Progression of Ankylosis Spondylitis by Regulating the Let-7i/SOST Axis

Zhang

et al. 2020

Front. Mol. Biosci.

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Ankylosis spondylitis (AS) is a disease mainly characterized by sacroiliac joint and spinal attachment point inflammation. Long non-coding RNA (lncRNA) plays a key role in the progression of many diseases. However, few studies have been conducted on the function of lncRNA maternally expressed gene 3 (MEG3) in AS. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to measure the relative levels of MEG3, microRNA let-7i, sclerostin (SOST), and inflammatory cytokines. Dual-luciferase reporter assay, RNA immunoprecipitation (RIP) assay and biotin-labeled RNA pull-down assay were used to confirm the interaction between MEG3 and let-7i or let-7i and SOST. In addition, western blot (WB) analysis was performed to detect the protein levels of osteogenesis markers and SOST. The expression levels of MEG3 and SOST were decreased and let-7i was increased in AS patients. MEG3 could interact with let-7i in AS fibroblasts, and let-7i overexpression reversed the suppressive effect of MEG3 upregulation on the inflammation and bone formation of AS. Additionally, let-7i could target SOST, and SOST silencing reversed the inhibitory effect of let-7i inhibitor or MEG3 overexpression on the inflammation and bone formation of AS. Furthermore, SOST expression was positively regulated by MEG3, while was negatively regulated by let-7i. Our results revealed that lncRNA MEG3 promoted SOST expression to restrain the progression of AS by sponging let-7i, which provided a treatment target for AS.

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Long non‑coding RNA NORAD promotes cell proliferation and glycolysis in non‑small cell lung cancer by acting as a sponge for miR‑136‑5p

Cited by 29 publications

References 29 publications

LINC00922 Accelerates the Proliferation, Migration and Invasion of Lung Cancer Via the miRNA-204/CXCR4 Axis

LINC00922 Accelerates the Proliferation, Migration and Invasion of Lung Cancer Via the miRNA-204/CXCR4 Axis

NORAD accelerates chemo-resistance of non-small-cell lung cancer via targeting at miR-129-1-3p/SOX4 axis

lncRNA MEG3 Suppresses the Progression of Ankylosis Spondylitis by Regulating the Let-7i/SOST Axis

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