ArticleJCI insight2024
Spon1+ inflammatory monocytes promote collagen remodeling and lung cancer metastasis through lipoprotein receptor 8 signaling.
Article in JCI insight, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
14 citing papers in PubMed.
- Extracellular Matrix Remodeling in Tumors: Forces Beyond Fibroblasts.Cancer research · 2026Article
- Multi-omics identification of SPON1-related risk model for predicting prognosis and drug response in ovarian cancer.Functional & integrative genomics · 2026Article
- Machine Learning-Guided Multi-Cohort Transcriptomic Profiling IdentifiesInternational journal of molecular sciences · 2026Article
- Spondin-1 Inhibits Odontoblastic Differentiation of Human Dental Pulp Stem Cells.Biomolecules · 2026Article
- Unveiling the developmental and tumor-suppressive roles of the p53 variant p53psi.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- A new mRNA antigen vaccine induces potent B and T cell responses and in vivo protection against SARS-CoV-2.NPJ vaccines · 2026Article
- A new mRNA antigen vaccine induces potent B and T cell responses andbioRxiv : the preprint server for biology · 2026Article
- Applying microfluidic technology to interpret the tumor immune microenvironment and cancer immunotherapy.Cancer biology & medicine · 2026Review
- Decoding adipocyte heterogeneity through single-nucleus transcriptomics unveils subtype-specific adipocytes orchestrate immunosuppressive niches in breast cancer.Journal for immunotherapy of cancer · 2026Article
- Single-nucleus transcriptomics identifies SPON1 as a candidate mediator of the anti-fibrotic effect ofAmerican journal of translational research · 2026Article
- The association between white blood cell count and relative risk of non-small cell lung cancer.Discover oncology · 2025Article
- White blood cell traits and lung cancer risk: a two-sample mendelian randomization analysis.Scientific reports · 2025Article
- The innate immune axis drives aortic dissection pathogenesis through inflammation and presents novel therapeutic targets.Frontiers in immunology · 2025Review
- Establishment and validation of a convenient and efficient screening tool for active pulmonary tuberculosis in lung cancer patients based on common parameters.Therapeutic advances in medical oncology · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors.
Funding
Abstract
Lung cancer is the leading cause of cancer-related deaths in the world, and non-small cell lung cancer (NSCLC) is the most common subset. We previously found that infiltration of tumor inflammatory monocytes (TIMs) into lung squamous carcinoma (LUSC) tumors is associated with increased metastases and poor survival. To further understand how TIMs promote metastases, we compared RNA-Seq profiles of TIMs from several LUSC metastatic models with inflammatory monocytes (IMs) of non-tumor-bearing controls. We identified Spon1 as upregulated in TIMs and found that Spon1 expression in LUSC tumors corresponded with poor survival and enrichment of collagen extracellular matrix signatures. We observed SPON1+ TIMs mediate their effects directly through LRP8 on NSCLC cells, which resulted in TGF-β1 activation and robust production of fibrillar collagens. Using several orthogonal approaches, we demonstrated that SPON1+ TIMs were sufficient to promote NSCLC metastases. Additionally, we found that Spon1 loss in the host, or Lrp8 loss in cancer cells, resulted in a significant decrease of both high-density collagen matrices and metastases. Finally, we confirmed the relevance of the SPON1/LRP8/TGF-β1 axis with collagen production and survival in patients with NSCLC. Taken together, our study describes how SPON1+ TIMs promote collagen remodeling and NSCLC metastases through an LRP8/TGF-β1 signaling axis.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.