ArticleBioResearch open access2012
cAMP Elevation Down-Regulates β3 Integrin and Focal Adhesion Kinase and Inhibits Leptin-Induced Migration of MDA-MB-231 Breast Cancer Cells.
Article in BioResearch open access, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 38 citations in OpenAlex.
- Multidimensional risk impact of obesity on breast cancer incidence, treatment, and prognosis.International journal of obesity (2005) · 2026Review
- The liver talks back: NPY orchestrates attraction of cancer cells and CHK2-dependent clonogenicity in the metastatic niche.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Indacaterol inhibits collective cell migration and IGDQ-mediated single cell migration in metastatic breast cancer MDA-MB-231 cells.Cell communication and signaling : CCS · 2023Article
- Control of adipogenic commitment by a STAT3-VSTM2A axis.American journal of physiology. Endocrinology and metabolism · 2021Article
- The Adipokine Component in the Molecular Regulation of Cancer Cell Survival, Proliferation and Metastasis.Pathology oncology research : POR · 2021Review
- MOB2 suppresses GBM cell migration and invasion via regulation of FAK/Akt and cAMP/PKA signaling.Cell death & disease · 2020Article
- AdipoRon Affects Cell Cycle Progression and Inhibits Proliferation in Human Osteosarcoma Cells.Journal of oncology · 2020Article
- Review
- Leptin-induced signaling pathways in cancer cell migration and invasion.Cellular oncology (Dordrecht, Netherlands) · 2019Review
- The Popeye domain containing gene family encoding a family of cAMP-effector proteins with important functions in striated muscle and beyond.Journal of muscle research and cell motility · 2019Review
- Obesity and Breast Cancer: Role of Leptin.Frontiers in oncology · 2019Review
- Linking obesity-induced leptin-signaling pathways to common endocrine-related cancers in women.Endocrine · 2019Review
- Leptin signaling axis specifically associates with clinical prognosis and is multifunctional in regulating cancer progression.Oncotarget · 2018Review
- Chemoresistance: Intricate Interplay Between Breast Tumor Cells and Adipocytes in the Tumor Microenvironment.Frontiers in endocrinology · 2018Review
- Dopaminergic Stimulation of Myeloid Antigen-Presenting Cells Attenuates Signal Transducer and Activator of Transcription 3-Activation Favouring the Development of Experimental Autoimmune Encephalomyelitis.Frontiers in immunology · 2018Article
- Dysregulation of POPDC1 promotes breast cancer cell migration and proliferation.Bioscience reports · 2017Article
- Collagen triple helix repeat containing 1 (CTHRC1) activates Integrin β3/FAK signaling and promotes metastasis in ovarian cancer.Journal of ovarian research · 2017Article
- EGFR expression is associated with cytoplasmic staining of CXCR4 and predicts poor prognosis in triple-negative breast carcinomas.Oncology letters · 2017Article
- Suberoylanilide hydroxamic acid-induced specific epigenetic regulation controls Leptin-induced proliferation of breast cancer cell lines.Oncotarget · 2017Article
- Leptin induces partial epithelial-mesenchymal transition in a FAK-ERK dependent pathway in MCF10A mammary non-tumorigenic cells.International journal of clinical and experimental pathology · 2017Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Breast cancer is one of the most common malignancies and a major cause of cancer death among women worldwide. The high mortality rate associated with breast cancer is mainly due to a propensity of the tumor to metastasize, even if small or undetectable. Given the relevant role of leptin in breast cancer growth and metastasis, novel strategies to counteract biological effects of this obesity-linked cytokine are warranted. Recently, we demonstrated that in MDA-MB-231 breast cancer cells, intracellular cAMP elevation completely abrogates both ERK1/2 and STAT3 phosphorylation in response to leptin. Very surprisingly, this provided evidence that when cAMP levels are increased, leptin drives cells towards apoptosis associated with a marked decrease of Bcl2 protein levels and accompanied by down-regulation of protein kinase A (PKA). The aim of the current study was to investigate the role of cAMP in leptin-associated motility of breast cancer cells. Here we show that cAMP elevation completely prevents leptin-induced migration of MDA-MB-231 breast cancer cells. Interestingly, the inhibition by cAMP-elevating agents of leptin-mediated cell migration is accompanied by a strong decrease of β3 integrin subunit and focal adhesion kinase (FAK) protein levels. Analysis of the underlying cAMP-dependent molecular mechanisms revealed that PKA blockers partly counteract the inhibition of leptin-induced migration and completely prevent the antiproliferative action by cAMP elevation. Moreover, a cAMP analogue that specifically activates Epac and not PKA has an inhibitory effect on leptin-induced cell migration as well. The present study confirms initial evidence for the efficacy of cAMP elevation against oncogenic effects of leptin, identifies β3 integrin subunit and FAK as proteins strongly down-regulated by cAMP elevation, and suggests that both cAMP/PKA- and cAMP/Epac-dependent pathways are involved in inhibition of leptin-induced migration of MDA-MB-231 breast cancer cells. The potential clinical significance and therapeutic applications of our data are discussed.
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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.