ArticleInternational journal of molecular medicine2012
A mechanism underlying the effects of polyunsaturated fatty acids on breast cancer.
Article in International journal of molecular medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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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.
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Who cites it
18 citing papers in PubMed, 36 citations in OpenAlex.
- THEM6 is a prognostic biomarker for breast cancer and is associated with immune infiltration.Scientific reports · 2023Article
- Multimodal imaging of metabolic activities for distinguishing subtypes of breast cancer.Biomedical optics express · 2023Article
- Butyrate reduces cellular magnesium absorption independently of metabolic regulation in Caco-2 human colon cells.Scientific reports · 2022Article
- TRP Channels as Molecular Targets to Relieve Endocrine-Related Diseases.Frontiers in molecular biosciences · 2022Review
- Emerging Roles for Ion Channels in Ovarian Cancer: Pathomechanisms and Pharmacological Treatment.Cancers · 2021Review
- Validation of plasma metabolites associated with breast cancer risk among Mexican Americans.Cancer epidemiology · 2020Article
- Targeting ferroptosis in breast cancer.Biomarker research · 2020Review
- Roles of endogenous ether lipids and associated PUFAs in the regulation of ion channels and their relevance for disease.Journal of lipid research · 2020Review
- The Calcium-Signaling Toolkit in Cancer: Remodeling and Targeting.Cold Spring Harbor perspectives in biology · 2019Review
- Breast cancer risk in relation to plasma metabolites among Hispanic and African American women.Breast cancer research and treatment · 2019Article
- Heterogeneity of fatty acid metabolism in breast cancer cells underlies differential sensitivity to palmitate-induced apoptosis.Molecular oncology · 2018Article
- Role of TRP ion channels in cancer and tumorigenesis.Seminars in immunopathology · 2016Review
- Oxidized derivative of docosahexaenoic acid preferentially inhibit cell proliferation in triple negative over luminal breast cancer cells.In vitro cellular & developmental biology. Animal · 2015Article
- TRP channels and STIM/ORAI proteins: sensors and effectors of cancer and stroma cell migration.British journal of pharmacology · 2014Review
- Plasma metabolomic profiles in breast cancer patients and healthy controls: by race and tumor receptor subtypes.Translational oncology · 2013Article
- Emerging role of TRP channels in cell migration: from tumor vascularization to metastasis.Frontiers in physiology · 2013Review
- Immunohistochemical characterization and functional identification of mammary gland telocytes in the self-assembly of reconstituted breast cancer tissue in vitro.Journal of cellular and molecular medicine · 2013Article
- Diet and nutrition in cancer survivorship and palliative care.Evidence-based complementary and alternative medicine : eCAM · 2013Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Breast cancer is the most frequent cancer in women. Evidence suggests that the polyunsaturated fatty acids (PUFAs), eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA) affect breast cancer proliferation, differentiation and prognosis. However, the mechanism still remains unclear. In this study, the expression of transient receptor potential canonical (TRPC)3 was detected throughout the cell cytoplasm and at the cell surface of MCF-7 cells. Ca(2+) entry was induced in these cells via activated TRPC3 by either the diacylglycerol analogue (OAG) or by intracellular Ca(2+) store depletion. TRPC-mediated Ca(2+) entry was inhibited by PUFAs including arachidonic acid (AA) and linolenic acid (LA) but not saturated fatty acids. Overexpression of the PUFA degradation enzyme, cyclooxygenase 2 (COX2), enhanced capacitative Ca(2+) entry. In addition, inhibition of COX2 reduced [Ca(2+)](i). Nevertheless, inhibition of TRPC reduced the cell cycle S phase and cell migration, implicating a functional role for TRP-mediated Ca(2+) entry in cell proliferation and invasion. Exogenous PUFA as well as a TRPC3 antagonist consistently attenuated breast cancer cell proliferation and migration, suggesting a mechanism in which PUFA restrains the breast cancer partly via its inhibition of TRPC channels. Additionally, our results also suggest that TRPC3 appears as a new mediator of breast cancer cell migration/invasion and represents a potential target for a new class of anticancer agent.
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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.