ArticleOncoTargets and therapy2019
Upregulation of SHIP2 participates in the development of breast cancer via promoting Wnt/β-catenin signaling.
Article in OncoTargets and therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 4 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
4 citing papers in PubMed, 7 citations in OpenAlex.
- SHIP2-PLK1 crosstalk promotes sensitivity to dual inhibition in esophageal squamous cell carcinoma.Molecular cancer · 2025Article
- SH2 domain-containing inositol 5-phosphatases support the survival of Burkitt lymphoma cells by promoting energy metabolism.Haematologica · 2024Article
- PTEN and Other PtdIns(3,4,5)PInternational journal of molecular sciences · 2020Review
- IQGAP2 Inhibits Migration and Invasion of Gastric Cancer Cells via Elevating SHIP2 Phosphatase Activity.International journal of molecular sciences · 2020Article
Corrections and comments
- Retracted
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeSrc homology 2-containing inositol 5-phosphatase 2 (
methodsThe BC tissue and adjacent cancerous tissue were obtained from BC patients who had underwent mastectomy. BC cells with either overexpression or knockdown of SHIP2 were analyzed to determine cell proliferation, migration, invasion and apoptosis using the CCK-8 assay, colony formation assay, scratch assay, transwell assay and flow cytometry, respectively. A rat BC xenograft model was constructed to explore the role of SHIP2 on tumor growth in vivo.
resultsThe expression levels of SHIP2 in BC tissues and cells were significantly higher than those in adjacent tissues and normal breast cells, respectively. Silencing SHIP2 suppressed BC cells proliferation and promoted apoptosis. Overexpression of SHIP2 enhanced the cells migration/invasion in BC. Moreover, SHIP2 participated in the Wnt/β-catenin pathway by regulating GSK-3β and its downstream genes. β-Catenin activator LiCl could significantly eliminate the effect of si-SHIP2 on BC cells. Moreover, overexpression of SHIP2 increased tumor volume and weight in rat model, and Wnt/β-catenin pathway inhibitor ICG001 reversed the promoting effect of SHIP2 on tumorigenesis.
conclusionUpregulation of SHIP2 could increase the migration, invasion, proliferation, and decrease apoptosis in BC cells. Moreover, SHIP2 participated in the progression of BC via activating the Wnt/β-catenin pathway.
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Registered trials
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