ArticleThe Journal of biological chemistry2013
G-protein-coupled receptor agonist BV8/prokineticin-2 and STAT3 protein form a feed-forward loop in both normal and malignant myeloid cells.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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
33 citing papers in PubMed, 61 citations in OpenAlex.
- Microenvironmental regulation of tumor-associated neutrophils in malignant glioma: from mechanism to therapy.Journal of neuroinflammation · 2024Review
- MRAP2a Binds and Modulates Activity and Localisation of Prokineticin Receptor 1 in Zebrafish.International journal of molecular sciences · 2024Article
- MRAP2 Inhibits β-Arrestin-2 Recruitment to the Prokineticin Receptor 2.Current issues in molecular biology · 2024Article
- Free-fatty acid receptor-1 (FFA1/GPR40) promotes papillary RCC proliferation and tumor growth via Src/PI3K/AKT/NF-κB but suppresses migration by inhibition of EGFR, ERK1/2, STAT3 and EMT.Cancer cell international · 2023Article
- S-1 eliminates MDSCs and enhances the efficacy of PD-1 blockade via regulation of tumor-derived Bv8 and S100A8 in thoracic tumor.Cancer science · 2023Article
- Review
- Identification and Characterization of a New Splicing Variant of Prokineticin 2.Life (Basel, Switzerland) · 2022Article
- Prokineticin-Receptor Network: Mechanisms of Regulation.Life (Basel, Switzerland) · 2022Review
- Review
- GPR4 signaling is essential for the promotion of acid-mediated angiogenic capacity of endothelial progenitor cells by activating STAT3/VEGFA pathway in patients with coronary artery disease.Stem cell research & therapy · 2021Article
- Vincristine- and bortezomib-induced neuropathies - from bedside to bench and back.Experimental neurology · 2021Review
- The balance of concentration between Prokineticin 2β and Prokineticin 2 modulates the food intake by STAT3 signaling.BBA advances · 2021Article
- Overview of the STAT-3 signaling pathway in cancer and the development of specific inhibitors.Oncology letters · 2020Review
- Metformin Ameliorates Diabetic Cardiomyopathy by Activating the PK2/PKR Pathway.Frontiers in physiology · 2020Article
- Review
- Activation of the NLRP3 Inflammasome Pathway by Prokineticin 2 in Testicular Macrophages of UropathogenicFrontiers in immunology · 2019Article
- Metformin Ameliorates Testicular Damage in Male Mice with Streptozotocin-Induced Type 1 Diabetes through the PK2/PKR Pathway.Oxidative medicine and cellular longevity · 2019Article
- Myeloid Derived Suppressor Cells Interactions With Natural Killer Cells and Pro-angiogenic Activities: Roles in Tumor Progression.Frontiers in immunology · 2019Review
- Novel imidazopyridine suppresses STAT3 activation by targeting SHP-1.Journal of enzyme inhibition and medicinal chemistry · 2018Article
- Clarithromycin expands CD11b+Gr-1+ cells via the STAT3/Bv8 axis to ameliorate lethal endotoxic shock and post-influenza bacterial pneumonia.PLoS pathogens · 2018Article
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 2 institutions in 1 country.
Funding
Abstract
backgroundSignaling pathways underlying BV8-mediated oncogenesis remain unknown.
resultsBV8-STAT3 forms a feed-forward loop in both normal and malignant myeloid cells and promotes tumor growth.
conclusionJAK2/STAT3 signaling plays critical roles in BV8-mediated myeloid cell-dependent oncogenesis. SIGNIFICANCE: This study identifies a novel role of BV8-STAT3 signaling in mediating cross-talk between tumor microenvironment and tumor cells. An important role of BV8 in mobilization of myeloid cells and myeloid cell-dependent angiogenesis has been established. Recently, it has also been shown that granulocyte colony-stimulating factor (G-CSF)-induced BV8 expression is STAT3 dependent in CD11b(+)Gr1(+) myeloid cells. However, the BV8 downstream signaling pathway(s) intrinsic to myeloid cells crucial for angiogenesis, and potentially also for development of cancers of myeloid origin, remains largely unknown. Here we show that BV8 activates STAT3, which is critical for regulating genes important for both tumor cell proliferation/survival and tumor angiogenesis, in both normal and malignant myeloid cells. Further, BV8-induced STAT3 activation requires Janus-activated kinase 2 (JAK2) activity as shown by both genetic and pharmacologic inhibition. Knocking down BV8 in human myeloid leukemia cells inhibits STAT3 activity and expression of STAT3 downstream angiogenic and pro-proliferation/survival genes, leading to a decrease in tumor cell viability. BV8 shRNA expressing leukemia cells exhibit reduced STAT3 activity and tumor growth in vivo. Taken together, we have delineated a signaling pathway downstream of BV8 that plays critical roles in both the tumor microenvironment and malignant myeloid cells for angiogenesis and tumor cell proliferation/survival.
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.