ArticleInternational journal of clinical and experimental pathology2015
Breast cancer cells promote osteoblastic differentiation via Sema 3A signaling pathway in vitro.
Article in International journal of clinical and experimental pathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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.
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Who cites it
5 citing papers in PubMed, 17 citations in OpenAlex.
- Expression of semaphorin 3A (SEMA3A) in breast cancer subtypes.Scientific reports · 2024Article
- Frequent Subgraph Mining of Functional Interaction Patterns Across Multiple Cancers.Pacific Symposium on Biocomputing. Pacific Symposium on Biocomputing · 2021Article
- Article
- Impact of semaphorin expression on prognostic characteristics in breast cancer.Breast cancer (Dove Medical Press) · 2018Review
- Decreased Expression of Semaphorin3A/Neuropilin-1 Signaling Axis in Apical Periodontitis.BioMed research international · 2017Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Breast cancer bone metastases are attributed to multiple cellular and molecular interactions between the cancer cells and the bone microenvironment. Some breast cancers (about 10%) manifest predominant osteoblastic bone metastases. However, the effects of cancer cell-produced factors on osteoblastic differentiation are not fully understood. Semaphorin 3A (Sema 3A) is a newly identified regulatory factor of bone rebuilding. In the present study, we demonstrated that human breast cancer MCF-7 cells, which preferentially form osteoblastic bone metastases, exhibited increased Sema 3A expression levels. We also found that MCF-7 cell-derived Sema 3A stimulated osteoblastic differentiation and nuclear β-catenin accumulation, and these effects could be blocked by shRNA Sema 3A or a Sema 3A-neutralizing antibody. In conclusion, our data suggest that MCF-7 cell-derived Sema 3A plays a causative role in osteoblastic bone metastases progression by stimulating osteoblastic differentiation.
Indexed as
Identifiers
25973043PMC4396274W2403273711What 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.