LncRNA NEAT1/miR-204/NUAK1 Axis is a Potential Therapeutic Target for Non-Small Cell Lung Cancer

Zhao, Mingming; Ge, Linyang; Yang, Liangfeng; Zheng, Haixia; Chen, Gang; Wu, Li-An; Shi, Shao-Ming; Wang, Nan; Hang, Yan-Ping

doi:10.2147/cmar.s277524

Cited by 14 publications

(7 citation statements)

References 43 publications

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“…Moreover, the 5-year survival rate of NSCLC patients still remains unsatisfactory. Studies have shown that the 5-year survival rate of late NSCLC patients is less than 15% [ 70 ]. The upregulation of NEAT1 in lung cancer tissues has been observed in several studies [ 68 , 69 , 71 ].…”

Section: Neat1 Sponges Micrornas and Stabilizes Mrnasmentioning

confidence: 99%

“…The upregulation of NEAT1 in lung cancer tissues has been observed in several studies [ 68 , 69 , 71 ]. NEAT1 can promote the proliferation and metastasis of NSCLC in vivo and in vitro by upregulating the expression of many oncogenes, including NAUK1, SULF1, SOX9, and E2F3 [ 68 , 69 , 70 , 71 ]. Higher NEAT1 levels are also associated with more lymph node metastasis, higher TNM grades, and a poor overall survival in patients [ 70 ].…”

Section: Neat1 Sponges Micrornas and Stabilizes Mrnasmentioning

confidence: 99%

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Molecular Interactions of the Long Noncoding RNA NEAT1 in Cancer

Zhang

et al. 2022

Cancers

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As one of the best-studied long noncoding RNAs, nuclear paraspeckle assembly transcript 1 (NEAT1) plays a pivotal role in the progression of cancers. NEAT1, especially its isoform NEAT1-1, facilitates the growth and metastasis of various cancers, excluding acute promyelocytic leukemia. NEAT1 can be elevated via transcriptional activation or stability alteration in cancers changing the aggressive phenotype of cancer cells. NEAT1 can also be secreted from other cells and be delivered to cancer cells through exosomes. Hence, elucidating the molecular interaction of NEAT1 may shed light on the future treatment of cancer. Herein, we review the molecular function of NEAT1 in cancer progression, and explain how NEAT1 interacts with RNAs, proteins, and DNA promoter regions to upregulate tumorigenic factors.

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Section: Neat1 Sponges Micrornas and Stabilizes Mrnasmentioning

confidence: 99%

Section: Neat1 Sponges Micrornas and Stabilizes Mrnasmentioning

confidence: 99%

Molecular Interactions of the Long Noncoding RNA NEAT1 in Cancer

Zhang

et al. 2022

Cancers

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“…Firstly, MDR1 acts in regulating multidrug resistance of BC cells, but this study did not determine whether astragaloside IV could improve drug resistance of BC cells by regulating MDR1. Secondly, earlier studies have shown that MDR1 was regulated by microRNA and lncRNA, which also underscores the significance of the establishment of a ceRNA network concerning astragaloside IV to monitor its effect on the drug resistance of BCCs [16].…”

Section: Discussionmentioning

confidence: 89%

Clinical effect of astragaloside IV on breast carcinoma cells based on MDR1: A randomised trial

Chen¹,

Zhuo²,

Yuan³

2021

Trop. J. Pharm Res

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Purpose: To study the clinical effect of astragaloside IV on breast carcinoma cells (BCCs), and its potential mechanisms with respect to multiple drug resistance-1 (MDR1)Methods: The cytotoxicity of astragaloside IV to BCCs was determined using CCK-8 test, and values of its half inhibitory concentration (IC50) were determined. Transwell assay and flow cytometry were performed to determine the effect of astragaloside (13 μg/mL) on cell invasion and apoptosis. The contents of MDR1 mRNA in BC tissues and cells were determined using real-time quantitative polymerase chain reaction (qRT-PCR), while the protein expression levels of MDR1 in BC cells were determined using western blot assay.Results: The IC50 of astragaloside IV for MCF-7 and MDA-MB-231 BCCs were 12.57 μg/mL and 13.91 μg/mL, respectively. Transwell experiment showed significantly inhibited invasive capacity and enhanced apoptotic potential of the BCCs after astragaloside IV intervention. However, invasive capacities of the BCCs were markedly enhanced, while their apoptotic capacities were inhibited after transfection with si-MDR1, when compared with controls (p < 0.05). Results of qRT-PCR revealed that the mRNA content of MDR1 in BC tissues and cells (0.42±0.11) was significantly lower than that in normal tissues (0.95±0.18; p < 0.05). Results from western blot assay revealed that the relative expression levels of MDR1 protein were decreased, with values of 0.21±0.05, 0.32±0.07 and 0.74±0.15 for MCF-10A, MCF-7, MAD-MB-231 and MCF-10A, respectively (p < 0.05).Conclusion: Astragaloside IV regulates the metastasis and apoptosis of BCCs through regulation of MDR1. It also inhibits cell invasion but enhances the apoptosis of BC cells transfected with si-MDR1. These results highlight the prospects of the compound for the treatment of BC.

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“…Numerous lncRNAs are dysregulated in NSCLC and have been associated with the regulation of malignant tumor characteristics ( 17 , 41 , 42 ). For example, MALAT1 ( 43 ), DGCR5 ( 44 ) and NCK1-AS1 ( 45 ) were found to be increased in NSCLC tissues and were associated with the oncogenicity of NSCLC.…”

Section: Discussionmentioning

confidence: 99%

Long non‑coding RNA LINC01748 exerts carcinogenic effects in non‑small cell lung cancer cell lines by regulating the microRNA‑520a‑5p/HMGA1 axis

Tan

et al. 2021

Int J Mol Med

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The important functions of long non-coding RNAs in the malignancy of non-small cell lung cancer (NSCLC) has been increasingly highlighted. However, whether LINC01748 functions in a crucial regulatory role still requires further research. The aim of the present study was to investigate the biological roles of LINC01748 in NSCLC. Furthermore, different experiments were utilized to investigate the mechanism of action of LINC01748 in 2 NSCLC cell lines. Reverse transcription-quantitative PCR was used to measure mRNA expression levels. Cell Counting Kit-8 assay, flow cytometry analysis and Transwell and Matrigel assays were also used to analyze, cell viability, apoptosis, and migration and invasion, respectively. A tumor xenograft model was used for in vivo experiments. RNA immunoprecipitation experiments, luciferase reporter assays and rescue experiments were used to investigate the mechanisms involved. Data from The Cancer Genome Atlas dataset and patients recruited into the present study showed that LINC01748 was overexpressed in NSCLC. Patients with high LINC01748 mRNA expression level had shorter overall survival rate compared with that in patients with low LINC01748 mRNA expression level. Then, knockdown of LINC01748 mRNA expression level reduced cell proliferation, migration and invasion, but increased cell apoptosis in vitro . Knockdown of LINC01748 also reduced tumor growth in vivo . Mechanistically, LINC01748 could act as a competing endogenous (ce)RNA to sponge microRNA(miR)-520a-5p, to increase the expression level of the target gene, high mobility group AT-hook 1 (HMGA1) in the NSCLC cell lines. Furthermore, rescue experiments illustrated that the functions exerted by LINC01748 knockdown were negated by miR-520a-5p inhibition or HMGA1 overexpression. In summary, LINC01748 acted as a ceRNA by sponging miR-520a-5p, leading to HMGA1 overexpression, thus increasing the aggressiveness of the NSCLC cells. Accordingly, targeting the LINC01748/miR-520a-5p/HMGA1 pathway may benefit NSCLC therapy.

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LncRNA NEAT1/miR-204/NUAK1 Axis is a Potential Therapeutic Target for Non-Small Cell Lung Cancer

Cited by 14 publications

References 43 publications

Molecular Interactions of the Long Noncoding RNA NEAT1 in Cancer

Molecular Interactions of the Long Noncoding RNA NEAT1 in Cancer

Clinical effect of astragaloside IV on breast carcinoma cells based on MDR1: A randomised trial

Long non‑coding RNA LINC01748 exerts carcinogenic effects in non‑small cell lung cancer cell lines by regulating the microRNA‑520a‑5p/HMGA1 axis

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