ArticleGenes & genomics2021
LncRNA HOTAIRM1 knockdown inhibits cell glycolysis metabolism and tumor progression by miR-498/ABCE1 axis in non-small cell lung cancer.
Article in Genes & genomics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 20 citations in OpenAlex.
- Nanomedicine novel strategies: deciphering the EV-metabolic axis as a natural nanocarrier network in lung cancer progression and cachexia.Journal of nanobiotechnology · 2026Review
- Role of HOXA transcript antisense RNA myeloid-specific 1 in cancer (Review).Oncology letters · 2026Review
- The Regulatory Role of LncRNAs in Modulating Autophagy and Drug Resistance in Non-Small-Cell Lung Cancer: Focus on Targeted Therapeutic Approaches.Biomolecules · 2025Review
- "Molecular pigeon" network of lncRNA and miRNA: decoding metabolic reprogramming in patients with lung cancer.Frontiers in oncology · 2025Review
- Glycolysis-associated lncRNAs in cancer energy metabolism and immune microenvironment: a magic key.Frontiers in immunology · 2024Review
- Extracellular vesicles and particles as mediators of long-range communication in cancer: connecting biological function to clinical applications.Extracellular vesicles and circulating nucleic acids · 2023Article
- Article
- Extracellular vesicles and particles impact the systemic landscape of cancer.The EMBO journal · 2022Review
- CircMCTP2 (has-circ-0000658) facilitates the proliferation and metastasis of bladder carcinoma through modulating the miR-498/murine double minute-2 axis.Bioengineered · 2022Article
- Targeting glycolysis in non-small cell lung cancer: Promises and challenges.Frontiers in pharmacology · 2022Review
- The Curcumin Analog Da0324 Inhibits the Proliferation of Gastric Cancer CellsJournal of Cancer · 2022Article
- Long Noncoding RNAs and Circular RNAs in the Metabolic Reprogramming of Lung Cancer: Functions, Mechanisms, and Clinical Potential.Oxidative medicine and cellular longevity · 2022Review
- Long noncoding RNA NR2F1-AS1 stimulates the tumorigenic behavior of non-small cell lung cancer cells by sponging miR-363-3p to increase SOX4.Open medicine (Warsaw, Poland) · 2022Article
- Identification and Validation of HOTAIRM1 as a Novel Biomarker for Oral Squamous Cell Carcinoma.Frontiers in bioengineering and biotechnology · 2021Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundNon-small cell lung cancer (NSCLC) is a major contributor of cancer-related mortality. Long non-coding RNAs (lncRNAs) are indicated to participate in the pathogenesis of NSCLC.
objectiveIn this research, the effects of lncRNA HOXA transcript antisense RNA, myeloid-specific 1 (HOTAIRM1) on NSCLC progression and underlying mechanism were revealed.
methodsThe expression levels of HOTAIRM1 and microRNA-498 (miR-498) were detected by quantitative real time polymerase chain reaction (qRT-PCR) in NSCLC tissues, cells or exosomes. The protein expression of CD63, CD81, hexokinase 2 (HK2) and ATP binding cassette subfamily E member 1 (ABCE1) was determined by western blot. Cell viability, apoptosis, migration and invasion were investigated by cell counting kit-8 (CCK-8), flow cytometry, transwell migration and invasion assays, respectively. Cell glycolysis metabolism was revealed by glucose uptake and lactate production assays and western blot analysis. The binding relationship between miR-498 and HOTAIRM1 or ABCE1 was predicted by DIANA-LncBase v2 and starBase online database, and identified by dual-luciferase reporter assay. The effects of HOTAIRM1 on NSCLC growth in vivo were revealed by in vivo tumor formation assay.
resultsHOTAIRM1 expression was dramatically upregulated, whereas miR-498 expression was significantly downregulated in NSCLC tissues cells or exosomes as compared to control groups. Mechanistically, HOTAIRM1 knockdown repressed cell viability, migration, invasion and glycolysis metabolism, whereas induced cell apoptosis in NSCLC; however, miR-498 inhibitor hindered these effects. Functionally, HOTAIRM1 functioned as a sponge of miR-498 and miR-498 targeted ABCE1. In addition, HOTAIRM1 silencing inhibited NSCLC growth in vivo by downregulating ABCE1 and upregulating miR-498 expression.
conclusionsHOTAIRM1 knockdown repressed cell glycolysis metabolism and tumor development by reducing ABCE1 expression through sponging miR-498 in NSCLC, which provided a theoretical basis for further studying NSCLC progression.
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