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Published on: January 21, 2018
Cardiac hormones for the treatment of cancer
1Division of Endocrinology, Diabetes and Metabolism, Departments of Medicine, Molecular Pharmacology and Physiology, James A. Haley VA Medical Center-151, University of South Florida Cardiac Hormone Center, Tampa, Florida 33612, USA. david.vesely@va.gov
Abstract:
Four cardiac hormones, namely atrial natriuretic peptide, vessel dilator, kaliuretic peptide, and long-acting natriuretic peptide, reduce up to 97% of all cancer cells in vitro. These four cardiac hormones eliminate up to 86% of human small-cell lung carcinomas, two-thirds of human breast cancers, and up to 80% of human pancreatic adenocarcinomas growing in athymic mice. Their anticancer mechanisms of action, after binding to specific receptors on cancer cells, include targeting the rat sarcoma-bound GTP (RAS) (95% inhibition)-mitogen-activated protein kinase kinase 1/2 (MEK 1/2) (98% inhibition)-extracellular signal-related kinase 1/2 (ERK 1/2) (96% inhibition) cascade in cancer cells. They also inhibit MAPK9, i.e. c-Jun N-terminal kinase 2. They are dual inhibitors of vascular endothelial growth factor (VEGF) and its VEGFR2 receptor (up to 89%). One of the downstream targets of VEGF is β-catenin, which they reduce up to 88%. The WNT pathway is inhibited up to 68% and secreted frizzled-related protein 3 decreased up to 84% by the four cardiac hormones. AKT, a serine/threonine protein kinase, is reduced up to 64% by the cardiac hormones. STAT3, a final 'switch' that activates gene expression that leads to malignancy, is decreased by up to 88% by the cardiac hormones. STAT3 is specifically decreased as they do not affect STAT1. There is a cross-talk between the RAS-MEK 1/2-ERK 1/2 kinase cascade, VEGF, β-catenin, WNT, JNK, and STAT pathways and each of these pathways is inhibited by the cardiac hormones.
Insights
Four cardiac hormones show significant anticancer activity, reducing up to 97% of cancer cells in vitro and in vivo. These hormones target key cancer pathways like RAS-MEK-ERK, VEGF, and STAT3, offering a novel therapeutic approach.
Area of Science:
- Cardiology
- Oncology
- Molecular Biology
Background:
- Cardiac hormones, including atrial natriuretic peptide, vessel dilator, kaliuretic peptide, and long-acting natriuretic peptide, have demonstrated potential in preclinical cancer research.
- Understanding the molecular mechanisms of these hormones is crucial for developing novel cancer therapies.
Purpose of the Study:
- To investigate the in vitro and in vivo anticancer efficacy of four cardiac hormones.
- To elucidate the molecular targets and pathways inhibited by these cardiac hormones in cancer cells.
Main Methods:
- In vitro and in vivo studies using various cancer cell lines and human tumor xenografts in athymic mice.
- Analysis of signaling pathways including RAS-MEK-ERK, VEGF, WNT, AKT, and STAT3 using molecular assays.
Main Results:
- Cardiac hormones reduced up to 97% of cancer cells in vitro and demonstrated significant efficacy against small-cell lung carcinoma, breast cancer, and pancreatic adenocarcinoma xenografts.
- Inhibition of key oncogenic pathways was observed: RAS-MEK-ERK (up to 98%), VEGF/VEGFR2 (up to 89%), β-catenin (up to 88%), WNT pathway (up to 68%), and STAT3 (up to 88%).
- Selective inhibition of STAT3 over STAT1 was noted, suggesting a specific anticancer mechanism.
Conclusions:
- Four cardiac hormones exhibit potent broad-spectrum anticancer activity.
- These hormones act by simultaneously inhibiting multiple critical cancer-related signaling pathways.
- Cardiac hormones represent a promising new class of anticancer agents with a multi-targeted mechanism of action.
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