ArticleThe Journal of biological chemistry2009
RGS16 inhibits breast cancer cell growth by mitigating phosphatidylinositol 3-kinase signaling.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
50 citing papers in PubMed, 1 synthesis or guideline pooled it.
- RGS Family Remodeling in Breast Cancer: A Meta-Analysis and Multi-Omics Profiling of Prognostic Biomarkers.Cancer medicine · 2026Pooled it
- RGS16-driven cancer-associated fibroblasts promote esophageal squamous cell carcinoma progression via the MDK-SDC1 axis-mediated intercellular crosstalk.Biology direct · 2025Article
- BHLHE40-mediated RGS16 upregulation: a driver propelling gastric cancer progression via ferroptosis suppression.Hereditas · 2025Article
- Dynamic regulation ofFrontiers in cell and developmental biology · 2025Article
- RGS4 controls airway hyperresponsiveness through GAP-independent mechanisms.The Journal of biological chemistry · 2024Article
- Phosphorylation of RGS16 at Tyr168 promote HBeAg-mediated macrophage activation by ERK pathway to accelerate liver injury.Journal of molecular medicine (Berlin, Germany) · 2024Article
- Defining the Effects of PKC Modulator HIV Latency-Reversing Agents on Natural Killer Cells.Pathogens & immunity · 2024Article
- Function and regulation of RGS family members in solid tumours: a comprehensive review.Cell communication and signaling : CCS · 2023Review
- RGS proteins and their roles in cancer: friend or foe?Cancer cell international · 2023Review
- RGS16 regulated by let-7c-5p promotes glioma progression by activating PI3K-AKT pathway.Frontiers of medicine · 2023Article
- Article
- Article
- RGS20 Promotes Tumor Progression through Modulating PI3K/AKT Signaling Activation in Penile Cancer.Journal of oncology · 2022Article
- Novel biomarkers predict prognosis and drug-induced neuroendocrine differentiation in patients with prostate cancer.Frontiers in endocrinology · 2022Article
- Functions of regulators of G protein signaling 16 in immunity, inflammation, and other diseases.Frontiers in molecular biosciences · 2022Review
- Metabolic acidosis regulates RGS16 and G protein signaling in osteoblasts.American journal of physiology. Renal physiology · 2021Article
- RGS proteins, GRKs, and beta-arrestins modulate G protein-mediated signaling pathways in asthma.Pharmacology & therapeutics · 2021Review
- RGS16 promotes glioma progression and serves as a prognostic factor.CNS neuroscience & therapeutics · 2020Article
- Article
- Anti-miRNA Oligonucleotide Therapy for Chondrosarcoma.Molecular cancer therapeutics · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
Aberrant activity of the phosphatidylinositol 3-kinase (PI3K) pathway supports growth of many tumors including those of breast, lung, and prostate. Resistance of breast cancer cells to targeted chemotherapies including tyrosine kinase inhibitors (TKI) has been linked to persistent PI3K activity, which may in part be due to increased membrane expression of epidermal growth factor (EGF) receptors (HER2 and HER3). Recently we found that proteins of the RGS (regulator of G protein signaling) family suppress PI3K activity downstream of the receptor by sequestering its p85alpha subunit from signaling complexes. Because a substantial percentage of breast tumors have RGS16 mutations and reduced RGS16 protein expression, we investigated the link between regulation of PI3K activity by RGS16 and breast cancer cell growth. RGS16 overexpression in MCF7 breast cancer cells inhibited EGF-induced proliferation and Akt phosphorylation, whereas shRNA-mediated extinction of RGS16 augmented cell growth and resistance to TKI treatment. Exposure to TKI also reduced RGS16 expression in MCF7 and BT474 cell lines. RGS16 bound the amino-terminal SH2 and inter-SH2 domains of p85alpha and inhibited its interaction with the EGF receptor-associated adapter protein Gab1. These results suggest that the loss of RGS16 in some breast tumors enhances PI3K signaling elicited by growth factors and thereby promotes proliferation and TKI evasion downstream of HER activation.
Indexed as
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.