ArticleBiochemical pharmacology2013
Identification of upregulated phosphoinositide 3-kinase γ as a target to suppress breast cancer cell migration and invasion.
Article in Biochemical pharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 26 citations in OpenAlex.
- Vascular Endothelial Cells Produce Coagulation Factors That Control Their Growth via Joint Protease-Activated Receptor and C5a Receptor 1 (CD88) Signaling.The American journal of pathology · 2022Article
- Varied functions of immune checkpoints during cancer metastasis.Cancer immunology, immunotherapy : CII · 2021Review
- Small Molecule Inhibitors Targeting GαCancers · 2020Article
- Targeting PIK3CG in Combination with Paclitaxel as a Potential Therapeutic Regimen in Claudin-Low Breast Cancer.Cancer management and research · 2020Article
- Novel role of Giα2 in cell migration: Downstream of PI3-kinase-AKT and Rac1 in prostate cancer cells.Journal of cellular physiology · 2018Article
- Noncanonical regulation of insulin-mediated ERK activation by phosphoinositide 3-kinase γ.Molecular biology of the cell · 2017Article
- Recent advances in the use of PI3K inhibitors for glioblastoma multiforme: current preclinical and clinical development.Molecular cancer · 2017Review
- Fibroblast growth factor receptor 4 (FGFR4) and fibroblast growth factor 19 (FGF19) autocrine enhance breast cancer cells survival.Oncotarget · 2016Article
- Signaling switch of the urotensin II vasosactive peptide GPCR: prototypic chemotaxic mechanism in glioma.Oncogene · 2015Article
- The PI3K/AKT/mTOR pathway is a potential predictor of distinct invasive and migratory capacities in human ovarian cancer cell lines.Oncotarget · 2015Article
- Manic fringe promotes a claudin-low breast cancer phenotype through notch-mediated PIK3CG induction.Cancer research · 2015Article
- Stat1 stimulates cap-independent mRNA translation to inhibit cell proliferation and promote survival in response to antitumor drugs.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Breast cancer regulated by Fringe.Oncoscience · 2015Article
- Epidermal growth factor-like module containing mucin-like hormone receptor 2 expression in gliomas.Journal of neuro-oncology · 2015Article
- Targeting p110gamma in gastrointestinal cancers: attack on multiple fronts.Frontiers in physiology · 2014Review
- Inhibition of HDAC1 and DNMT1 modulate RGS10 expression and decrease ovarian cancer chemoresistance.PloS one · 2014Article
- Molecular determinants of PI3Kγ-mediated activation downstream of G-protein-coupled receptors (GPCRs).Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- 3-Phosphoinositide-dependent protein kinase-1 as an emerging target in the management of breast cancer.Cancer management and research · 2013Review
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Metastasis is the major cause of breast cancer mortality. We recently reported that aberrant G-protein coupled receptor (GPCR) signaling promotes breast cancer metastasis by enhancing cancer cell migration and invasion. Phosphatidylinositol 3-kinase γ (PI3Kγ) is specifically activated by GPCRs. The goal of the present study was to determine the role of PI3Kγ in breast cancer cell migration and invasion. Immunohistochemical staining showed that the expression of PI3Kγ protein was significantly increased in invasive human breast carcinoma when compared to adjacent benign breast tissue or ductal carcinoma in situ. PI3Kγ was also detected in metastatic breast cancer cells, but not in normal breast epithelial cell line or in non-metastatic breast cancer cells. In contrast, PI3K isoforms α, β and δ were ubiquitously expressed in these cell lines. Overexpression of recombinant PI3Kγ enhanced the metastatic ability of non-metastatic breast cancer cells. Conversely, migration and invasion of metastatic breast cancer cells were inhibited by a PI3Kγ inhibitor or by siRNA knockdown of PI3Kγ but not by inhibitors or siRNAs of PI3Kα or PI3Kβ. Lamellipodia formation is a key step in cancer metastasis, and PI3Kγ blockade disrupted lamellipodia formation induced by the activation of GPCRs such as CXC chemokine receptor 4 and protease-activated receptor 1, but not by the epidermal growth factor tyrosine kinase receptor. Taken together, these results indicate that upregulated PI3Kγ conveys the metastatic signal initiated by GPCRs in breast cancer cells, and suggest that PI3Kγ may be a novel therapeutic target for development of chemotherapeutic agents to prevent breast cancer metastasis.
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