ArticleInternational journal of molecular sciences2022
Crosstalk between β-Catenin and CCL2 Drives Migration of Monocytes towards Glioblastoma Cells.
Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 35 citations in OpenAlex.
- The role of SH3RF2 in lung squamous cell carcinoma and M2 polarization: insights into LZTS2 ubiquitination.Biology direct · 2025Article
- Navigating the brain: Harnessing endogenous cellular hitchhiking for targeting neoplastic and neuroinflammatory diseases.Asian journal of pharmaceutical sciences · 2025Review
- Preclinical evaluation of DC-CIK cells as potentially effective immunotherapy model for the treatment of glioblastoma.Scientific reports · 2025Article
- Advance in therapies targeting tumor-associated macrophages in ovarian cancer.Frontiers in immunology · 2025Review
- M2-like tumor-associated macrophage-secreted CCL2 facilitates gallbladder cancer stemness and metastasis.Experimental hematology & oncology · 2024Article
- Wnt signaling regulates chemokine production and cell migration of circulating human monocytes.Cell communication and signaling : CCS · 2024Article
- Muscarinic receptor drug trihexyphenidyl can alter growth of mesenchymal glioblastomaFrontiers in pharmacology · 2024Article
- Silencing HOXC13 exerts anti-prostate cancer effects by inducing DNA damage and activating cGAS/STING/IRF3 pathway.Journal of translational medicine · 2023Article
- Systematic integration of m6A regulators and autophagy-related genes in combination with long non-coding RNAs predicts survival in glioblastoma multiforme.Scientific reports · 2023Article
- Editorial to Special Issue "Glioblastoma: Recapitulating the Key Breakthroughs and Future Perspective".International journal of molecular sciences · 2023Article
- Pro- vs. Anti-Inflammatory Features of Monocyte Subsets in Glioma Patients.International journal of molecular sciences · 2023Article
- Multiomics integration reveals the effect of Orexin A on glioblastoma.Frontiers in pharmacology · 2023Article
- Barriers to overcoming immunotherapy resistance in glioblastoma.Frontiers in medicine · 2023Review
- Glioma-associated microglia/macrophages (GAMs) in glioblastoma: Immune function in the tumor microenvironment and implications for immunotherapy.Frontiers in immunology · 2023Review
- WNT/β-Catenin-Mediated Resistance to Glucose Deprivation in Glioblastoma Stem-like Cells.Cancers · 2022Article
- Inflammatory Breast Cancer: The Secretome of HCMVFrontiers in oncology · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 6 institutions in 5 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Isocitrate dehydrogenase (IDH)-wildtype glioblastoma (GBM) is a fast growing and highly heterogeneous tumor, often characterized by the presence of glioblastoma stem cells (GSCs). The plasticity of GSCs results in therapy resistance and impairs anti-tumor immune response by influencing immune cells in the tumor microenvironment (TME). Previously, β-catenin was associated with stemness in GBM as well as with immune escape mechanisms. Here, we investigated the effect of β-catenin on attracting monocytes towards GBM cells. In addition, we evaluated whether CCL2 is involved in β-catenin crosstalk between monocytes and tumor cells. Our analysis revealed that shRNA targeting β-catenin in GBMs reduces monocytes attraction and impacts CCL2 secretion. The addition of recombinant CCL2 restores peripheral blood mononuclear cells (PBMC) migration towards medium (TCM) conditioned by shβ-catenin GBM cells. CCL2 knockdown in GBM cells shows similar effects and reduces monocyte migration to a similar extent as β-catenin knockdown. When investigating the effect of CCL2 on β-catenin activity, we found that CCL2 modulates components of the Wnt/β-catenin pathway and alters the clonogenicity of GBM cells. In addition, the pharmacological β-catenin inhibitor MSAB reduces active β-catenin, downregulates the expression of associated genes and alters CCL2 secretion. Taken together, we showed that β-catenin plays an important role in attracting monocytes towards GBM cells in vitro. We hypothesize that the interactions between β-catenin and CCL2 contribute to maintenance of GSCs via modulating immune cell interaction and promoting GBM growth and recurrence.
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.