ArticleCancer discovery2016
Stromal Expression of miR-143/145 Promotes Neoangiogenesis in Lung Cancer Development.
Article in Cancer discovery, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 97 papers.
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Who cites it
97 citing papers in PubMed, 185 citations in OpenAlex.
- Distinct migratory dendritic cell subsets cooperate to prime tissue-resident memory-like CD8⁺ T cells in mouse tumors.Nature communications · 2026Article
- Antagonistic roles of histone H3 lysine methyltransferases dictate tumor immune surveillance.Nature communications · 2026Article
- The miR-143/145 cluster in prostate cancer: molecular regulation, context-dependent functions, and medical implications.Biology direct · 2026Review
- PRMT5 inhibitors actively promote metastatic progression of lung adenocarcinoma.bioRxiv : the preprint server for biology · 2026Article
- Targeting CAMK1D-engineered nanoactivator suppresses cancer stem cell maintenance and immune evasion in enzalutamide-resistant prostate cancer.Theranostics · 2026Article
- CAMK1D activates AMPK/PINK1/Parkin-dependent mitophagy to promote enzalutamide resistance in prostate cancer.Cell death & disease · 2025Article
- Comorbidity of hypertension and lung cancer: interplay of genetics and environment.Discover oncology · 2025Review
- The PRMT5-splicing axis is a critical oncogenic vulnerability that regulates detained intron splicing.iScience · 2025Article
- Lung Cancer-Intrinsic SOX2 Expression Mediates Resistance to Checkpoint Blockade Therapy by Inducing Treg-Dependent CD8+ T-cell Exclusion.Cancer immunology research · 2025Article
- Review
- Plasma miR-145-5p Levels and Risk of Future Cancer-Results from the HUNT Study.International journal of molecular sciences · 2025Article
- Mechanisms of miRNAs (MicroRNAs) and Their Expression in Gastric Cancer.Archives of Razi Institute · 2025Review
- The miR-941/FOXN4/TGF-β feedback loop induces N2 polarization of neutrophils and enhances tumor progression of lung adenocarcinoma.Frontiers in immunology · 2025Article
- Aberrant cytoplasmic expression of UHRF1 restrains the MHC-I-mediated anti-tumor immune response.Nature communications · 2024Article
- Dendritic cell-targeted therapy expands CD8 T cell responses to bona-fide neoantigens in lung tumors.Nature communications · 2024Article
- EMID2 is a novel biotherapeutic for aggressive cancers identified by in vivo screening.Journal of experimental & clinical cancer research : CR · 2024Article
- ALCAM-mediated cDC1 CD8 T cells interactions are suppressed in advanced lung tumors.Oncoimmunology · 2024Article
- KEAP1 mutation in lung adenocarcinoma promotes immune evasion and immunotherapy resistance.Cell reports · 2023Article
- Pro-tumorigenic role of lnc-ZNF30-3 as a sponge counteracting miR-145-5p in prostate cancer.Biology direct · 2023Article
- Stanniocalcin 1 promotes lung metastasis of breast cancer by enhancing EGFR-ERK-S100A4 signaling.Cell death & disease · 2023Article
37 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
unlabelledThe two unrelated miRNAs miR-143 and miR-145, coexpressed from the miR-143/145 cluster, have been proposed to act as tumor suppressors in human cancer, and therapeutic benefits of delivering miR-143 and miR-145 to tumors have been reported. In contrast, we found that tumor-specific deletion of miR-143/145 in an autochthonous mouse model of lung adenocarcinoma did not affect tumor development. This was consistent with the lack of endogenous miR-143/145 expression in normal and transformed lung epithelium. Surprisingly, miR-143/145 in the tumor microenvironment dramatically promoted tumor growth by stimulating the proliferation of endothelial cells. Loss of miR-143/145 in vivo led to derepression of the miR-145 target CAMK1D, an inhibitory kinase, which when overexpressed prevents mitotic entry of endothelial cells. As a consequence, tumors in miR-143/145-deficient animals exhibited diminished neoangiogenesis, increased apoptosis, and their expansion was limited by the tumor's ability to co-opt the alveolar vasculature. These findings demonstrate that stromal miR-143/145 promotes tumorigenesis and caution against the use of these miRNAs as agents in cancer therapeutics. SIGNIFICANCE: This study shows that miR-143/145 expressed from the tumor microenvironment stimulates neoangiogenesis and supports tumor expansion in the lung, demonstrating a surprising role for the putative tumor suppressor miRNA cluster in promoting tumorigenesis. We propose inhibition of miR-143/145 as a therapeutic avenue to modulate tumor neoangiogenesis.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.