ArticleThe Journal of pathology2015
Loss of RUNX3 expression promotes cancer-associated bone destruction by regulating CCL5, CCL19 and CXCL11 in non-small cell lung cancer.
Article in The Journal of pathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 45 citations in OpenAlex.
- RUNX transcription factors: biological functions and implications in cancer.Clinical and experimental medicine · 2024Review
- Study on Potential Differentially Expressed Genes in Idiopathic Pulmonary Fibrosis by Bioinformatics and Next-Generation Sequencing Data Analysis.Biomedicines · 2023Article
- Decoding the immune landscape following hip fracture in elderly patients: unveiling temporal dynamics through single-cell RNA sequencing.Immunity & ageing : I & A · 2023Article
- A two-sample Mendelian randomization analysis: causal association between chemokines and pan-carcinoma.Frontiers in genetics · 2023Article
- Increased joint loading induces subchondral bone loss of the temporomandibular joint via the RANTES-CCRs-Akt2 axis.JCI insight · 2022Article
- Article
- Does CCL19 act as a double-edged sword in cancer development?Clinical and experimental immunology · 2022Review
- CCL5 production in lung cancer cells leads to an altered immune microenvironment and promotes tumor development.Oncoimmunology · 2022Article
- Identification of marker genes and cell subtypes in castration-resistant prostate cancer cells.Journal of Cancer · 2021Article
- The YY1/miR-548t-5p/CXCL11 signaling axis regulates cell proliferation and metastasis in human pancreatic cancer.Cell death & disease · 2020Article
- Inducers, Attractors and Modulators of CD4Frontiers in immunology · 2020Review
- lncRNA MT1JP Suppresses Biological Activities of Breast Cancer Cells in vitro and in vivo by Regulating the miRNA-214/RUNX3 Axis.OncoTargets and therapy · 2020Article
- CCL28-induced RARβ expression inhibits oral squamous cell carcinoma bone invasion.The Journal of clinical investigation · 2019Article
- Expression ofOncology letters · 2019Article
- miR-301a promotes lung tumorigenesis by suppressing Runx3.Molecular cancer · 2019Article
- Intra-CA1 Administration of Minocycline Alters the Expression of Inflammation-Related Genes in Hippocampus of CCI Rats.Frontiers in molecular neuroscience · 2019Article
- Mast cells induce epithelial-to-mesenchymal transition and migration in non-small cell lung cancer through IL-8/Wnt/β-catenin pathway.Journal of Cancer · 2019Article
- Genome-wide DNA methylation profiling shows a distinct epigenetic signature associated with lung macrophages in cystic fibrosis.Clinical epigenetics · 2018Article
- Emerging role of RUNX3 in the regulation of tumor microenvironment.BMB reports · 2018Review
- Hypoxia negatively affects senescence in osteoclasts and delays osteoclastogenesis.Journal of cellular physiology · 2018Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Non-small cell lung cancer (NSCLC) frequently metastasizes to bone, which is associated with significant morbidity and a dismal prognosis. RUNX3 functions as a tumour suppressor in lung cancer and loss of expression occurs more frequently in invasive lung adenocarcinoma than in pre-invasive lesions. Here, we show that RUNX3 and RUNX3-regulated chemokines are linked to NSCLC-mediated bone resorption. Notably, the receptor activator of nuclear factor-κB ligand (RANKL)/osteoprotegerin (OPG) ratio, an index of osteoclastogenic stimulation, was significantly increased in human osteoblastic cells treated with conditioned media derived from RUNX3-knockdown NSCLC cells. We aimed to identify RUNX3-regulated factors that modify the osteoblastic RANKL/OPG ratio and found that RUNX3 knockdown led to CCL5 up-regulation and down-regulation of CCL19 and CXCL11 in NSCLC cells. Tumour size was noticeably increased and more severe osteolytic lesions were induced in the calvaria and tibiae of mice that received RUNX3-knockdown cells. In response to RUNX3 knockdown, serum and tissue levels of CCL5 increased, whereas CCL19 and CXCL11 decreased. Furthermore, CCL5 increased the proliferation, migration, and invasion of lung cancer cells in a dose-dependent manner; however, CCL19 and CXCL11 did not show any significant effects. The RANKL/OPG ratio in osteoblastic cells was increased by CCL5 but reduced by CCL19 and CXCL11. CCL5 promoted osteoclast differentiation, but CCL19 and CXCL11 reduced osteoclastogenesis in RANKL-treated bone marrow macrophages. These findings suggest that RUNX3 and related chemokines are useful markers for the prediction and/or treatment of NSCLC-induced bone destruction.
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