LncRNA NUTM2A‐AS1 positively modulates TET1 and HIF‐1A to enhance gastric cancer tumorigenesis and drug resistance by sponging miR‐376a

Wang, Ji; Yu, Ziyang; Wang, Jun; Shen, Yidan; Qiu, Junlan; Zhuang, Zhixiang

doi:10.1002/cam4.3544

Cited by 34 publications

(25 citation statements)

References 37 publications

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“…However, the underlying molecular mechanism of the effects of NUTM2A-AS1 in lung cancer has not been reported, to the best of our knowledge. A previous study demonstrated that programmed death-ligand 1 partially rescued NUTM2A-AS1- and miR-376a-regulated gastric cancer (GC) cell tumorigenesis and drug resistance ( 30 ). In addition, miR-376a was recently identified to be associated with NUTM2A-AS1 and found to be critical for NUTM2A-AS1-induced tumorigenesis ( 30 ).…”

Section: Discussionmentioning

confidence: 99%

“…A previous study demonstrated that programmed death-ligand 1 partially rescued NUTM2A-AS1- and miR-376a-regulated gastric cancer (GC) cell tumorigenesis and drug resistance ( 30 ). In addition, miR-376a was recently identified to be associated with NUTM2A-AS1 and found to be critical for NUTM2A-AS1-induced tumorigenesis ( 30 ). Moreover, lncRNA realizes its function by regulating miRNA/mRNA expression ( 31 ).…”

Section: Discussionmentioning

confidence: 99%

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Knockdown of lncRNA NUTM2A‑AS1 inhibits lung adenocarcinoma cell viability by regulating the miR‑590‑5p/METTL3 axis

2021

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Lung adenocarcinoma (LUAD) is the leading cause of cancer-related mortality worldwide. Long non-coding RNA (lncRNA) NUT family member 2A antisense RNA 1 (NUTM2A-AS1) is dysregulated in LUAD; however, its role in this disease remains unclear. The present study aimed to identify the underlying molecular mechanism of the effect of lncRNA NUTM2A-AS1 in LUAD by exploring whether lncRNA NUTM2A-AS1 could affect LUAD cell proliferation and apoptosis through the microRNA (miR)-590-5p/methyltransferase 3, N6-adenosine-methyltransferase complex catalytic subunit (METTL3) axis. miR-590-5p was predicted and verified as the direct target of NUTM2A-AS1 using bioinformatics analysis and a dual luciferase reporter assay. The expression levels of NUTM2A-AS1 and miR-590-5p in lung cancer cells, and the effects of NUTM2A-AS1 on cell viability and apoptosis were determined using MTT assays and flow cytometry, respectively. Reverse transcription-quantitative PCR analysis revealed that the expression levels of NUTM2A-AS1 were significantly upregulated, while those of miR-590-5p were significantly downregulated, in lung cancer cells compared with the control epithelial cells. NUTM2A-AS1 knockdown inhibited NCI-H23 cell viability and induced apoptosis by upregulating miR-590-5p expression. Moreover, the function and regulatory mechanism of miR-590-5p in LUAD were also investigated. It was determined that miR-590-5p could interact with METTL3, and further analysis of the expression levels of METTL3 in lung cancer cells demonstrated that METTL3 was significantly upregulated in NCI-H23 and A549 cells compared with the control cells. In addition, miR-590-5p inhibited NCI-H23 cell viability and induced apoptosis by downregulating METTL3 expression. In conclusion, the findings of the present study suggested that NUTM2A-AS1 knockdown may inhibit LUAD progression by regulating the miR-590-5p/METTL3 axis. These results may provide insight into the mechanisms underlying the tumorigenesis of LUAD and offer a new treatment strategy for the disease.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Knockdown of lncRNA NUTM2A‑AS1 inhibits lung adenocarcinoma cell viability by regulating the miR‑590‑5p/METTL3 axis

2021

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“…Besides, more and more evidence suggested that higher glycolysis may contribute to the development of drug resistance in multiple tumors, including TNBC. HIF-1α plays a critical role in the regulation of glycolysis of cancer cells, has been demonstrated to be related to chemoresistance in many kinds of cancer cells 46,47 . We demonstrated in this study that downregulation of ANRIL decreased HIF-1α-dependent glycolysis.…”

Section: Discussionmentioning

confidence: 99%

Long Non-Coding RNA ANRIL Promotes Doxorubicin Resistance in Triple-Negative Breast Cancer via Suppressing Glycolysis Through the MicroRNA-125a/ENO Pathway

Ma¹,

Zhao²,

Zhang³

et al. 2021

Preprint

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BackgroundBreast cancer is the main cause of death among women worldwide. More and more long non-coding RNAs (lncRNAs) have been identified as oncogenes or tumor suppressors during cancer development. However, whether ANRIL is involved in drug resistance in triple-negative breast cancer (TNBC) has not been investigated. MethodsLuciferase reporter assay was conducted to verify the binding of miR-125a and ANRIL. RT-PCR and western blot were performed to detect the expression of miR-125a, ANRIL and ENO1. Gene silence and overexpression experiments as well as CCK-8 and colony formation assays on TNBC cell lines were performed to determine the regulation of molecular pathways. Glycolysis analysis was performed with Seahorse extracellular flux methodology. ResultsANRIL expression in TNBC patients and TNBC cells was examined and we found that ANRIL expression was upregulated in both TNBC patients and TNBC cell lines. Knockdown of ANRIL increased the cytotoxic effect of ADR and inhibited HIF-1α-dependent glycolysis in TNBC cells. In addition, we found that ANRIL negatively regulated miR-125a expression in TNBC cell lines. Besides, a dual-luciferase reporter assay proved ANRIL functioned as a sponger of miR-125a. Further investigation revealed that ENO1 was a target of miR-125a and positively regulated by ANRIL in TNBC cells. Additionally, ANRIL upregulation reversed miR-125-mediated inhibition on HIF-1α-dependent glycolysis in TNBC cells. More notably, 2-deoxy-glucose (2-DG) attenuated ANRIL-induced increase of drug resistance in TNBC cells. ConclusionsTaken together, our study was the first to identify that knockdown of ANRIL plays an active role in overcoming the drug resistance in TNBC by inhibiting glycolysis through the miR-125a/ENO1 pathway, which maybe serve useful for the development of novel therapeutic targets.

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“…HIF-1α induces the expression of miR-27a, which is closely associated with MDR in GC ( Zhao et al, 2015 ). By binding to miR-376a, the lncRNA Nutm2a-AS1 positively modulates GC formation and drug resistance through the regulation of HIF-1α ( Wang et al, 2020c ).…”

Section: The Mechanism Of Resistance To Chemotherapy or Radiotherapy Of Ncrnas For Gastric Cancermentioning

confidence: 99%

The Molecular Roles and Clinical Implications of Non-Coding RNAs in Gastric Cancer

Yue

Lin

Qiu

et al. 2021

Front. Cell Dev. Biol.

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Gastric cancer (GC) is one of the most common malignancies in the world. It is also the fifth most common cancer in China. In recent years, a large number of studies have proved that non-coding RNAs (ncRNAs) can regulate cell proliferation, invasion, metastasis, apoptosis, and angiogenesis. NcRNAs also influence the therapeutic resistance of gastric cancer. NcRNAs mainly consist of miRNAs, lncRNAs and circRNAs. In this paper, we summarized ncRNAs as biomarkers and therapeutic targets for gastric cancer, and also reviewed their role in clinical trials and diagnosis. We sum up different ncRNAs and related moleculars and signaling pathway in gastric cancer, like Bcl-2, PTEN, Wnt signaling. In addition, the potential clinical application of ncRNAs in overcoming chemotherapy and radiotherapy resistance in GC in the future were also focused on.

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LncRNA NUTM2A‐AS1 positively modulates TET1 and HIF‐1A to enhance gastric cancer tumorigenesis and drug resistance by sponging miR‐376a

Abstract: This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

Cited by 34 publications

References 37 publications

Knockdown of lncRNA NUTM2A‑AS1 inhibits lung adenocarcinoma cell viability by regulating the miR‑590‑5p/METTL3 axis

Knockdown of lncRNA NUTM2A‑AS1 inhibits lung adenocarcinoma cell viability by regulating the miR‑590‑5p/METTL3 axis

Long Non-Coding RNA ANRIL Promotes Doxorubicin Resistance in Triple-Negative Breast Cancer via Suppressing Glycolysis Through the MicroRNA-125a/ENO Pathway

The Molecular Roles and Clinical Implications of Non-Coding RNAs in Gastric Cancer

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