ArticleJournal of cell communication and signaling2012
CCN5/WISP-2: A micromanager of breast cancer progression.
Article in Journal of cell communication and signaling, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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.
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
30 citing papers in PubMed, 50 citations in OpenAlex.
- Expression and clinical significance of CCN5 and the oestrogen receptor in advanced breast cancer.BMC women's health · 2025Article
- Modified mRNA-MediatedInternational journal of molecular sciences · 2024Article
- Expressions and clinical significance of CCN5 and E-cadherin in primary and recurrent lesions of breast cancer.Frontiers in genetics · 2024Article
- CCN proteins: opportunities for clinical studies-a personal perspective.Journal of cell communication and signaling · 2023Review
- The role of CCNs in controlling cellular communication in the tumor microenvironment.Journal of cell communication and signaling · 2023Review
- Potential Role of CCN Proteins in Breast Cancer: Therapeutic Advances and Perspectives.Current oncology (Toronto, Ont.) · 2021Review
- Article
- CCN5 activation by free or encapsulated EGCG is required to render triple-negative breast cancer cell viability and tumor progression.Pharmacology research & perspectives · 2021Article
- Clinical significance of CCN5 and mutant p53 in primary and recurrent lesions of breast cancer.American journal of translational research · 2021Article
- WISP2 promotes cell proliferation via targeting ERK and YAP in ovarian cancer cells.Journal of ovarian research · 2020Article
- Signaling Pathways Induced by Leptin during Epithelial⁻Mesenchymal Transition in Breast Cancer.International journal of molecular sciences · 2018Review
- Racial disparity in breast cancer: can it be mattered for prognosis and therapy.Journal of cell communication and signaling · 2018Review
- CCN5/WISP2 and metabolic diseases.Journal of cell communication and signaling · 2018Review
- CCN5 in alveolar epithelial proliferation and differentiation during neonatal lung oxygen injury.Journal of cell communication and signaling · 2018Article
- Leptin-induced ER-α-positive breast cancer cell viability and migration is mediated by suppressing CCN5-signaling via activating JAK/AKT/STAT-pathway.BMC cancer · 2018Article
- CCN5/WISP-2 restores ER-∝ in normal and neoplastic breast cells and sensitizes triple negative breast cancer cells to tamoxifen.Oncogenesis · 2017Article
- Deficiency of CCN5/WISP-2-Driven Program in breast cancer Promotes Cancer Epithelial cells to mesenchymal stem cells and Breast Cancer growth.Scientific reports · 2017Article
- CCN family of proteins: critical modulators of the tumor cell microenvironment.Journal of cell communication and signaling · 2016Article
- Human pancreatic cancer progression: an anarchy among CCN-siblings.Journal of cell communication and signaling · 2016Article
- Exosomes in carcinogenesis: molecular palkis carry signals for the regulation of cancer progression and metastasis.Journal of cell communication and signaling · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The gain of plasticity by a subset of cancer cells is a unique but common sequence of cancer progression from epithelial phenotype to mesenchymal phenotype (EMT) that is followed by migration, invasion and metastasis to a distant organ, and drug resistance. Despite multiple studies, it is still unclear how cancer cells regulate plasticity. Recent studies from our laboratory and others' proposed that CCN5/WISP-2, which is found intracellularly (in the nucleus and cytoplasm) and extracellularly, plays a negative regulator of plasticity. It prevents the EMT process in breast cancer cells as well as pancreatic cancer cells. Multiple genetic insults, including the gain of p53 mutations that accumulate over the time, may perturb CCN5 expression in non-invasive breast cancer cells, which ultimately helps cells to gain invasive phenotypes. Moreover, emerging evidence indicates that several oncogenic lesions such as miR-10b upregulation and activation of TGF-β-signaling can accumulate during CCN5 crisis in breast cancer cells. Collectively, these studies indicate that loss of CCN5 activity may promote breast cancer progression; application of CCN5 protein may represent a novel therapeutic intervention in breast cancer and possibly pancreatic cancer.
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.