ArticleOncology reports2019
Bradykinin promotes proliferation, migration, and invasion of cervical cancer cells through STAT3 signaling pathways.
Article in Oncology reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.
What it found
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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
9 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.
- Factor XII-A New Therapeutic Target? A Systematic Review.International journal of molecular sciences · 2026Pooled it
- Therapeutic Targeting of the Bradykinin B2 Receptor in Immunological and Vascular Diseases: Insights from Kinin Biology to Clinical Outcomes.Clinical reviews in allergy & immunology · 2026Review
- Article
- Metabolomics analysis reveals resembling metabolites between humanized γδ TCR mice and human plasma.Scientific reports · 2024Article
- Kinin Receptors B1 and B2 Mediate Breast Cancer Cell Migration and Invasion by Activating the FAK-Src Axis.International journal of molecular sciences · 2024Article
- Levels of Angiotensin and Kinin Metabolite Peptides Related to COVID-19 Severity.ACS pharmacology & translational science · 2024Article
- Bradykinin-bradykinin receptor (B1R) signalling is involved in the blood-brain barrier disruption in moyamoya disease.Journal of cellular and molecular medicine · 2023Article
- Tumor vessel co-option: The past & the future.Frontiers in oncology · 2022Review
- The Bradykinin-BDKRB1 Axis RegulatesCancers · 2020Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It has been reported recently that bradykinin (BK) is involved in the regulation of various processes in cancer cells. However, its role and underlying mechanism of action in cervical cancer (CC) are still unknown. In the present study, it was revealed that BK promoted proliferation, migration, and invasion of CC cells, whereas bradykinin B2 receptor antagonist HOE140 had the inverse effect. Furthermore, it was confirmed that overexpression of bradykinin B2 receptor (B2R) facilitated the proliferation, migration, and invasion of BK‑treated CC cells, while knockdown of B2R had the opposite effect. Mechanistically, the present results revealed that the BK/B2R‑induced biological function of CC cells occured by activating STAT3 signaling pathways, and that knockdown of B2R or B2R antagonist had the opposite effects. Moreover, it was demonstrated that BK/B2R facilitated CC cell migration and invasion by upregulating the expression of the STAT3‑regulated products MMP2 and MMP9, while downregulating the expression of the pro‑apoptotic protein cleaved caspase‑9. Thus, the present findings revealed that BK promoted CC cell proliferation, migration, and invasion by binding to B2R via STAT3 signaling pathways.
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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.