ArticleBreast cancer (Dove Medical Press)2025
ANXA2 Regulates RANKL-Induced Osteoclast Differentiation Through STAT3 Signaling in Breast Cancer.
Article in Breast cancer (Dove Medical Press), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- The Neuro-Bone Axis in Metastatic Progression: Innervation, Neuro-Immune-Osteoclast Crosstalk, and Therapeutic Opportunities.Biology · 2026Review
- Research Progress on Signaling Pathways in Breast Cancer Bone Metastasis.Oncology research · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Bone metastasis affects nearly 70% of patients with advanced breast cancer, significantly influencing patient survival. Osteoclasts play a crucial role in osteolysis and the proliferation of bone tumor cell metastasis. Although previous studies have established Anxa2 as a critical factor in the invasion and metastasis of breast cancer, its involvement in bone metastasis remains poorly understood. Methods: The correlation between ANXA2 expression and survival was analyzed in breast cancer cohorts. Enrichment analysis was performed to explore ANXA2-associated signaling pathways. RAW264.7 cells were induced to differentiate into osteoclasts using conditioned media from breast cancer cells, and osteoclastogenesis was quantified using the TRAP assay. Breast cancer cell lines with either Anxa2 overexpression or knockdown were established to assess the impact on osteoclastogenesis. The mRNA and protein expression levels were analyzed by RT-PCR and Western blot. The role of STAT3 in regulating RANKL expression was evaluated using a dual luciferase reporter assay. Results: ANXA2 was significantly upregulated in breast cancer patients and associated with poor survival. GO and KEGG analyses revealed that ANXA2 substantially modulated signaling pathways involved in bone metastasis. Furthermore, ANXA2 notably enhanced the differentiation of RAW264.7 cells into osteoclasts and upregulated genes associated with osteoclast differentiation. Additional investigation showed that ANXA2 markedly activated the STAT3 signaling pathway and increased RANKL expression. The dual luciferase reporter assay demonstrated that STAT3 directly bound to the -1804 region of the RANKL promoter, thereby regulating RANKL expression. Conclusion: This study identifies ANXA2 as a key regulator of osteoclast differentiation through STAT3-mediated upregulation of RANKL, driving bone metastasis in breast cancer. These results highlight the potential of targeting the ANXA2/STAT3/RANKL axis as a therapeutic strategy to combat bone metastasis.
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.