ArticleJournal of Cancer2015
Deregulation of RGS17 Expression Promotes Breast Cancer Progression.
Article in Journal of Cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
What it found
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.
- RGS Family Remodeling in Breast Cancer: A Meta-Analysis and Multi-Omics Profiling of Prognostic Biomarkers.Cancer medicine · 2026Pooled it
- Tumor-secreted RGS17 impairs CD8 + T cell function in lung adenocarcinoma through affecting glucose metabolism mediated by PI3K/AKT pathway.Discover oncology · 2025Article
- NRF2 activation by cysteine as a survival mechanism for triple-negative breast cancer cells.Oncogene · 2024Article
- Regulators of G-Protein Signaling (RGS) in Sporadic and Colitis-Associated Colorectal Cancer.International journal of molecular sciences · 2024Review
- RGS proteins and their roles in cancer: friend or foe?Cancer cell international · 2023Review
- Fragment-Based Nuclear Magnetic Resonance Screen against a Regulator of G Protein Signaling Identifies a Binding "Hot Spot".Chembiochem : a European journal of chemical biology · 2021Article
- Probing the mutational landscape of regulators of G protein signaling proteins in cancer.Science signaling · 2020Article
- Regulator of G-protein signaling (RGS) proteins as drug targets: Progress and future potentials.The Journal of biological chemistry · 2019Review
- High-resolution structure of RGS17 suggests a role for CaThe Journal of biological chemistry · 2019Article
- Tannic Acid Induces Endoplasmic Reticulum Stress-Mediated Apoptosis in Prostate Cancer.Cancers · 2018Article
- RGS17 inhibits tumorigenesis and improves 5-fluorouracil sensitivity in nasopharyngeal carcinoma.OncoTargets and therapy · 2018Article
- miR-203 inhibits cell proliferation, invasion, and migration of non-small-cell lung cancer by downregulating RGS17.Cancer science · 2017Article
- Natural Products Discovered in a High-Throughput Screen Identified as Inhibitors of RGS17 and as Cytostatic and Cytotoxic Agents for Lung and Prostate Cancer Cell Lines.Journal of natural products · 2017Article
- Development of a bimolecular luminescence complementation assay for RGS: G protein interactions in cells.Analytical biochemistry · 2017Article
- Regulator of G Protein Signaling 17 as a Negative Modulator of GPCR Signaling in Multiple Human Cancers.The AAPS journal · 2016Review
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveA high level of RGS17 expression is observed in diverse human cancers and correlates with tumor progression. Herein, we aim to investigate its expression and function in breast cancer.
methodsThe expression of RGS17 was detected by immunohistochemical analysis and western blot analysis. The level of miR-32 expression was investigated by qRT-PCR. Western blot analysis was used to determine the relationship between RGS17 and miR-32. A series of loss or gain of function assays was performed to measure the effects of RGS17 or miR-32 on tumor migration, invasion, and proliferation.
resultsCompared to that in normal breast specimen, the expression of RGS17 had a significantly higher expression level in breast cancer tissues and cell lines. Although the potential relationship of RGS17 expression with clinicopathological features was not observed, there was a significant correlation of RGS17 expression with p63 expression. In cells, inhibition of RGS17 expression impaired cell migration, invasion, and proliferation. Further, RGS17 was identified as a direct and functional target of miR-32. Overexpression of miR-32 in cells could decrease the expression of RGS17 and inhibit cell migration, invasion, and proliferation. In contrast, ectopic expression of RGS17 could attenuate phenotypes caused by miR-32 overexpression.
conclusionThe expression of RGS17 was upregulated in breast cancer, which could enhance cell migration, invasion, and proliferation. Moreover, the RGS17 was identified as a target of miR-32. Our results suggest that RGS17 might play an important role in breast cancer progression and could be a potential target for human breast cancer treatment.
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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.