ArticleOncology letters2018
Overexpression of ROD1 inhibits invasion of breast cancer cells by suppressing the translocation of β-catenin into the nucleus.
Article in Oncology letters, 2018. 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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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.
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Who cites it
5 citing papers in PubMed, 6 citations in OpenAlex.
- Polypyrimidine Tract Binding Protein: A Universal Player in Cancer Development.Current molecular medicine · 2024Review
- Podocyte specific deletion of PKM2 ameliorates LPS-induced podocyte injury through beta-catenin.Cell communication and signaling : CCS · 2022Article
- New Insights Into PTBP3 in Human Cancers: Immune Cell Infiltration, TMB, MSI, PDCD1 and m6A Markers.Frontiers in pharmacology · 2022Article
- Constructing and validating a diagnostic nomogram for multiple sclerosis via bioinformatic analysis.3 Biotech · 2021Article
- PTBP3 promotes migration of non-small cell lung cancer through regulating E-cadherin in EMT signaling pathway.Cancer cell international · 2020Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The incidence of breast cancer is increasing throughout the world. Although significant progress has been made in diagnostic techniques and targeted therapies, the prognosis of breast cancer remains poor. Regulator of differentiation 1 (ROD1) may inhibit the development of several types of cancer. However, the role of ROD1 in breast cancer cells remains unknown. In the present study, western blot analysis and reverse transcription-quantitative polymerase chain reaction revealed that expression of ROD1 was significantly reduced in breast cancer cells. Overexpression of ROD1 reduced the proliferation rate, demonstrated using a Cell Counting Kit-8 assay. Additionally, the overexpression of ROD1 decreased the invasiveness of breast cancer cells, indicating that ROD1 may serve as a tumor suppressor. Additionally, the data suggested that ROD1 significantly suppressed the activity of Wnt luciferase reporter (TOP Flash) in MDA-MB-231 cells. Furthermore, it was demonstrated that ROD1 may interact with β-catenin by using co-immunoprecipitation, resulting in suppression of β-catenin migration into the nucleus. Notably, ROD1 demonstrated its anticancer effect by decreasing β-catenin (Y333) phosphorylation in a nude mouse xenograft model. Overexpression of ROD1 may downregulate Ki67 protein levels, as determined by immunohistochemistry. These results indicated that ROD1 may be used as a therapeutic target in patients with breast cancer.
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