ArticleDiscover oncology2022
Tumor-derived exosomal HOTAIRM1 regulates SPON2 in CAFs to promote progression of lung adenocarcinoma.
Article in Discover oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 17 citations in OpenAlex.
- LncRNA interactomes and co-methylation in breast cancer regulation.Biomolecules & biomedicine · 2025Article
- MicroRNAs as Regulators, Biomarkers, and Therapeutic Targets in Autism Spectrum Disorder.Molecular neurobiology · 2025Review
- Exosomal LncRNAs and CircRNAs in lung cancer: Emerging regulators and potential therapeutic targets.Non-coding RNA research · 2024Review
- Single cell transcriptomic analysis reveals tumor immune infiltration by NK cells gene signature in lung adenocarcinoma.Heliyon · 2024Article
- Long non-coding RNAs are involved in the crosstalk between cancer-associated fibroblasts and tumor cells.Frontiers in immunology · 2024Review
- Non-coding RNAs and exosomal non-coding RNAs in lung cancer: insights into their functions.Frontiers in cell and developmental biology · 2024Review
- Unraveling the Connection: Extracellular Vesicles and Non-Small Cell Lung Cancer.International journal of nanomedicine · 2024Review
- p63: a crucial player in epithelial stemness regulation.Oncogene · 2023Review
- Long Non-Coding RNAs as Emerging Targets in Lung Cancer.Cancers · 2023Review
- Knockdown of SPON2 inhibits the growth of triple-negative breast cancer.Frontiers in oncology · 2023Article
- Exosomal Long Noncoding RNAs in NSCLC: Dysfunctions and Clinical Potential.Journal of Cancer · 2023Review
- Construction of IL-1 signalling pathway correlation model in lung adenocarcinoma and association with immune microenvironment prognosis and immunotherapy: Multi-data validation.Frontiers in immunology · 2023Article
- The biological functions and related signaling pathways of SPON2.Frontiers in oncology · 2023Review
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 1 country.
Funding
Abstract
objectiveSPON2 is one of the extracellular matrix proteins, which is closely related to the progression of a variety of tumors including non-small cell lung cancer (NSCLC), but its upstream regulation mechanism remains unclear. Our research aims to find the specific regulatory pathway of SPON2 by exploring the potential crosstalk between tumor cells and cancer-associated fibroblasts (CAFs) in tumor microenvironment (TME) of NSCLC.
methodsWe analyzed T1 lung adenocarcinoma samples from TCGA and screened extracellular matrix proteins that indicate poor prognosis. Expression level of SPON2 was verified by qPCR in clinical samples. The exosomes of NSCLC cell supernatant were extracted and identified by nanoparticle tracking analysis (NTA) and transmission electron microscope, western blots. The exosomes and CAFs were co-cultured, and cell migration and Matrigel invasion assay were used to evaluate the effect of CAFs on the migration and invasion of NSCLC cells. The interaction between LncRNA and miRNA was verified by Targetscan prediction, luciferase reporter assay, and RNA binding protein immunoprecipitation (RIP).
resultsWe found that the expression of SPON2 was up-regulated in clinical T1a stage NSCLC patients. The expression of lnc HOTAIRM1 (HOTAIRM1) in exosomes secreted by NSCLC tissues increased. After exosomal HOTAIRM1 entered CAFs, HOTAIRM1 can adsorb miR-328-5p to up-regulate the expression of SPON2 in CAFs. Up-regulation of SPON2 in CAFs could promote the migration and invasion of NSCLC cells.
conclusionTumor-derived exosomal HOTAIRM1 can transfer into CAFs and competitively adsorb miR-328-5p, and regulate the SPON2 expression of CAFs cells, ultimately promote the progression of NSCLC. The discovery of this regulatory pathway can provide a new potential therapeutic target for the diagnosis and treatment of NSCLC.
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