A mechanism underlying the effects of polyunsaturated fatty acids on breast cancer

Zhang, Hao; Zhou, Lei; Shi, Wei; Song, Ning; Yu, Karu; Gu, Yuchun

doi:10.3892/ijmm.2012.1022

Cited by 35 publications

(18 citation statements)

References 56 publications

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“…Moreover, the activity of TRPC3 has been suggested to be regulated by polyunsaturated fatty acids (PUFAs). This finding could be a new approach to regulate calcium influx in breast cancer cells [86]. Exogenous PUFA inhibited TRPC3-dependent calcium entry evoked by thapsigargin.…”

Section: Calcium Channels Migration and Metastasis In Breast Cancermentioning

confidence: 76%

Plasma membrane calcium channels in cancer: Alterations and consequences for cell proliferation and migration

Déliot

Constantin

2015

Biochimica et Biophysica Acta (BBA) - Biomembranes

159

140

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The study of calcium channels in molecular mechanisms of cancer transformation is still a novel area of research. Several studies, mostly conducted on cancer cell lines, however support the idea that a diversity of plasma membrane channels participates in the remodeling of Ca2+ homeostasis, which regulates various cancer hallmarks such as uncontrolled multiplication and increase in migration and invasion abilities. However few is still understood concerning the intracellular signaling cascades mobilized by calcium influx participating to cancer cell behavior. This review intends to gather some of these pathways dependent on plasma membrane calcium channels and described in prostate, breast and lung cancer cell lines. In these cancer cell types, the calcium channels involved in calcium signaling pathways promoting cancer behaviors are mostly non-voltage activated calcium channels and belong to the TRP superfamily (TRPC, TPRPV and TRPM families) and the Orai family. TRP and Orai channels are part of many signaling cascades involving the activation of transmembrane receptors by extracellular ligand from the tumor environment. TRPV can sense changes in the physical and chemical environment of cancer cells and TRPM7 are stretch activated and sensitive to cholesterol. Changes in activation and or expression of plasma-membrane calcium channels affect calcium-dependent signaling processes relevant to tumorigenesis. The studies cited in this review suggest that an increase in plasma membrane calcium channel expression and/or activity sustain an elevated calcium entry (constitutive or under the control of extracellular signals) promoting higher cell proliferation and migration in most cases. A variety of non-voltage-operated calcium channels display change expression and/or activity in a same cancer type and cooperate to the same process relevant to cancer cell behavior, or can be involved in a different sequence of events during the tumorigenesis. This article is part of a Special Issue entitled: Membrane channels and transporters in cancers.

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Section: Calcium Channels Migration and Metastasis In Breast Cancermentioning

confidence: 76%

Plasma membrane calcium channels in cancer: Alterations and consequences for cell proliferation and migration

Déliot

Constantin

2015

Biochimica et Biophysica Acta (BBA) - Biomembranes

159

140

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“…For example, oleate increases proliferation, migration and invasion in MDA‐MB‐231 cells (Hardy et al ., 2005; Wu et al ., 2017) and MCF‐7 cells (Soto‐Guzman et al ., 2008), but this effect on MCF‐7 cells is not always observed (Hardy et al ., 2005). Other literature has described the effects of other FA species such as the omega‐3 or omega‐6 FAs on BrCa cell biology (Mansara et al ., 2015; Tiwari et al ., 1991; Zhang et al ., 2012). However, the breadth of FA diversity, driven by differences in chain length and saturation/desaturation status, and combinations of different FA species continue to challenge the broader understanding of the influence of FAs has on BrCa cell proliferation, migration, and invasion.…”

Section: Discussionmentioning

confidence: 99%

Heterogeneity of fatty acid metabolism in breast cancer cells underlies differential sensitivity to palmitate‐induced apoptosis

et al. 2018

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Breast cancer (BrCa) metabolism is geared toward biomass synthesis and maintenance of reductive capacity. Changes in glucose and glutamine metabolism in BrCa have been widely reported, yet the contribution of fatty acids (FAs) in BrCa biology remains to be determined. We recently reported that adipocyte coculture alters MCF‐7 and MDA‐MB‐231 cell metabolism and promotes proliferation and migration. Since adipocytes are FA‐rich, and these FAs are transferred to BrCa cells, we sought to elucidate the FA metabolism of BrCa cells and their response to FA‐rich environments. MCF‐7 and MDA‐MB‐231 cells incubated in serum‐containing media supplemented with FAs accumulate extracellular FAs as intracellular triacylglycerols (TAG) in a dose‐dependent manner, with MDA‐MB‐231 cells accumulating more TAG. The differences in TAG levels were a consequence of distinct differences in intracellular partitioning of FAs, and not due to differences in the rate of FA uptake. Specifically, MCF‐7 cells preferentially partition FAs into mitochondrial oxidation, whereas MDA‐MB‐231 cells partition FAs into TAG synthesis. These differences in intracellular FA handling underpin differences in the sensitivity to palmitate‐induced lipotoxicity, with MDA‐MB‐231 cells being highly sensitive, whereas MCF‐7 cells are partially protected. The attenuation of palmitate‐induced lipotoxicity in MCF‐7 cells was reversed by inhibition of FA oxidation. Pretreatment of MDA‐MB‐231 cells with FAs increased TAG synthesis and reduced palmitate‐induced apoptosis. Our results provide novel insight into the potential influences of obesity on BrCa biology, highlighting distinct differences in FA metabolism in MCF‐7 and MDA‐MB‐231 cells and how lipid‐rich environments modulate these effects.

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“…Multiple pathways have been proposed to explain how DHA has also been reported to induce apoptosis via multiple pathways (Berquin et al 2008; Sun et al 2008; Blanckaert et al 2010; Kang et al 2010; Ravacci et al 2013). The mechanism of DHA remains unclear and controversial (Gago-Dominguez et al 2003; Stripp et al 2003; Schley et al 2007; Zhang et al 2012). Furthermore, no mechanism has been identified to explain why triple-negative breast cancer cells are more sensitive to DHA, 4-OH-DHA, and 4-OXO-DHA treatment.…”

Section: Discussionmentioning

confidence: 99%

Oxidized derivative of docosahexaenoic acid preferentially inhibit cell proliferation in triple negative over luminal breast cancer cells

Pogash

El‐Bayoumy

Amin

et al. 2014

In Vitro Cell.Dev.Biol.-Animal

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Omega-3 polyunsaturated fatty acids (PUFAs) exert an anticancer effect by affecting multiple cellular mechanisms leading to inhibition of proliferation and induction of apoptosis. It is well known that breast cancer comprises distinct molecular subtypes which differ in their responsiveness to therapeutic and preventive agents. We tested the hypothesis that n-3FA may preferentially affect triple-negative breast cancer cells for which no targeted intervention is presently available. The in vitro antiproliferative effects of n-3 PUFA docosahexaenoic acid (DHA) and its metabolite, 4-OH-DHA as well as its putative metabolite 4-OXO-DHA, were tested in five triple-negative human basal breast cell lines at different stages of transformation (MCF-10F, trMCF, bsMCF, MDA-MB-231, and BT-549) and three luminal breast cancer cell lines (MCF-7, T-47D, and SK-BR-3). Cell proliferation was measured with the tetrazolium MTT (3-(4,5-dimethylthiazolyl-2)-2,5-diphenyltetrazolium bromide) assay. DHA and its oxidized derivatives significantly inhibited cell proliferation (20–90% reduction) of both basal and luminal breast cancer cell lines. The inhibitory effect was more pronounced on triple-negative basal breast cancer cell lines as compared to luminal breast cancer cell lines after 4-OXO-DHA treatment. Our data provide novel information regarding the preferential antitumor effect of oxidized derivatives of DHA on basal type breast cancer.

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A mechanism underlying the effects of polyunsaturated fatty acids on breast cancer

Cited by 35 publications

References 56 publications

Plasma membrane calcium channels in cancer: Alterations and consequences for cell proliferation and migration

Plasma membrane calcium channels in cancer: Alterations and consequences for cell proliferation and migration

Heterogeneity of fatty acid metabolism in breast cancer cells underlies differential sensitivity to palmitate‐induced apoptosis

Oxidized derivative of docosahexaenoic acid preferentially inhibit cell proliferation in triple negative over luminal breast cancer cells

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