An overview of the effect of linoleic and conjugated‐linoleic acids on the growth of several human tumor cell lines

Maggiora, Marina; Bologna, Mauro; Cerù, Maria Paola; Possati, L; Angelucci, Adriano; Cimini, Annamaria; Miglietta, Antonella; Bozzo, Francesca; Margiotta, Chiara; Muzio, Giuliana; Canuto, Rosa Angela

doi:10.1002/ijc.20519

Cited by 110 publications

(95 citation statements)

References 42 publications

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“…Linoleic acid and conjugated linoleic acid -CLA (geometrical and positional stereoisomer) have an impact on tumor development. In gliomas linoleic acid, different effects were exerted, ranging from inhibitory to neutral (Maggiora et al, 2004). Cimini et al (2005) studied the effects of CLA on cell growth, differentiation, and death of a human glioblastoma cell line (ADF).…”

Section: Discussionmentioning

confidence: 99%

Chemical composition and antioxidant activity of beebread, and its influence on the glioblastoma cell line (U87MG)

Markiewicz‐Żukowska¹,

Naliwajko²,

Bartosiuk³

et al. 2013

Journal of Apicultural Science

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A b s t r a c t Beebread is processed pollen stored in the cells of the honeycomb, with the addition of various enzymes and honey, which undergoes lactic acid fermentation. Ethanolic extracts (EBBs) were obtained from three different samples of beebread from Poland. Assays were carried out for the determination of chemical composition (GC/MS), for the total phenolic content, and for the antioxidant and cytotoxic activities. The effects of beebread extracts (10, 20, 30, 50, 100 µg/mL) on the viability of the glioblastoma cell line (U87MG) were studied after 24 h, 48 h, and 72 h. Our results indicated a time-dependent inhibitory effect on the viability of U87MG cells treated EBB. The main inhibitory effect of EBB was observed after 72 h; EBB treatment decreased cell viability to 49 -66%.

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Section: Discussionmentioning

confidence: 99%

Chemical composition and antioxidant activity of beebread, and its influence on the glioblastoma cell line (U87MG)

Markiewicz‐Żukowska¹,

Naliwajko²,

Bartosiuk³

et al. 2013

Journal of Apicultural Science

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“…In contrast, PPAR␥ and PPAR␦ agonists have been extensively studied to evaluate their anticancer effects because of their antiproliferative, proapoptotic, antiapoptotic, and differentiation-promoting activity (4). However, recent studies have revealed the expression of PPAR␣ in tumor cells (5,6), and PPAR␣ ligands suppress the growth of several cancer lines, including colon, breast, endometrial and skin, in vitro (7)(8)(9)(10). PPAR␣ ligands also suppress the metastatic potential of melanoma cells in vitro and in vivo (11,12).…”

mentioning

confidence: 99%

PPARα agonist fenofibrate suppresses tumor growth through direct and indirect angiogenesis inhibition

Panigrahy

Kaipainen

Huang

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

244

206

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Angiogenesis and inflammation are central processes through which the tumor microenvironment influences tumor growth. We have demonstrated recently that peroxisome proliferatoractivated receptor (PPAR)␣ deficiency in the host leads to overt inflammation that suppresses angiogenesis via excess production of thrombospondin (TSP)-1 and prevents tumor growth. Hence, we speculated that pharmacologic activation of PPAR␣ would promote tumor growth. Surprisingly, the PPAR␣ agonist fenofibrate potently suppressed primary tumor growth in mice. This effect was not mediated by cancer-cell-autonomous antiproliferative mechanisms but by the inhibition of angiogenesis and inflammation in the host tissue. Although PPAR␣-deficient tumors were still susceptible to fenofibrate, absence of PPAR␣ in the host animal abrogated the potent antitumor effect of fenofibrate. In addition, fenofibrate suppressed endothelial cell proliferation and VEGF production, increased TSP-1 and endostatin, and inhibited corneal neovascularization. Thus, both genetic abrogation of PPAR␣ as well as its activation by ligands cause tumor suppression via overlapping antiangiogenic pathways. These findings reveal the potential utility of the well tolerated PPAR␣ agonists beyond their use as lipid-lowering drugs in anticancer therapy. Our results provide a mechanistic rationale for evaluating the clinical benefits of PPAR␣ agonists in cancer treatment, alone and in combination with other therapies. stroma ͉ inflammation ͉ fibrates ͉ microenvironment P eroxisome proliferator-activated receptors (PPARs) are a family of nuclear receptors comprising three isoforms, PPAR␣, PPAR␦, and PPAR␥, which act as ligand-activated transcriptional factors. PPARs play key roles in energy homeostasis by modulating glucose and lipid metabolism and transport (1). PPAR␣ is also critical in inflammation (2) and is the molecular target of the fibrate class of drugs, such as fenofibrate, which act as agonistic ligands of PPAR␣.Long-term administration of certain PPAR␣ agonists (clofibrate and WY14643) induces hepatocarcinogenesis in rodents but not in humans (3). Consequently, PPAR␣ has not been established as a molecular target for cancer therapy by its agonistic ligands. In contrast, PPAR␥ and PPAR␦ agonists have been extensively studied to evaluate their anticancer effects because of their antiproliferative, proapoptotic, antiapoptotic, and differentiation-promoting activity (4). However, recent studies have revealed the expression of PPAR␣ in tumor cells (5, 6), and PPAR␣ ligands suppress the growth of several cancer lines, including colon, breast, endometrial and skin, in vitro (7-10). PPAR␣ ligands also suppress the metastatic potential of melanoma cells in vitro and in vivo (11,12). Furthermore, PPAR␣ ligands decrease tumor development in murine colon carcinogenesis (7). Clofibric acid inhibits the growth of human ovarian cancer in mice (13). Most recently, the PPAR␣ agonist WY14643 suppresses tumorigenesis in a PPAR␣-dependent manner (14).Together, these data suggest that PPAR...

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“…[9][10][11][12] In previous studies, we have reported that CLA inhibits the growth of different human cancer cell lines, among which are breast cancer cells. 13 CLA's suppression of cell proliferation was in some cases positively correlated with inhibition of mitogen-activated protein kinase/extracellular signal-related kinase, 14,15 but the underlying mechanisms by which CLA interfered with cell proliferation have not been fully clarified. Interestingly, it has been recently reported that CLA could modulate lipid metabolism, cellular proliferation and differentiation through the activation of peroxisome proliferator-activated receptors (PPARs).…”

mentioning

confidence: 99%

“…18,29,30 In a previous study we reported that the effects of CLA on cell growth or death in prostate and bladder cancer cells seemed to involve the PPARg isoform. 13 More recently, it has been suggested that the PPARsignaling pathway is connected with the b-catenin pathway. 31 b-catenin is an intracellular multifunctional protein that binds to either E-cadherin or APC proteins; in a complex with the transmembrane receptor E-cadherin, b-catenin becomes plasma membrane-associated and mediates intercellular adhesion.…”

mentioning

confidence: 99%

Involvement of PPARγ and E‐cadherin/β‐catenin pathway in the antiproliferative effect of conjugated linoleic acid in MCF‐7 cells

Bocca

Bozzo

Francica

et al. 2007

Intl Journal of Cancer

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Conjugated linoleic acid (CLA) is a naturally occurring fatty acid, which has been shown to exert beneficial effects against breast carcinogenesis. It has been reported that CLA could modulate cellular proliferation and differentiation through the activation of peroxisome proliferator-activated receptors (PPARs). Among different PPAR isotypes, PPARc is involved in growth inhibition of transformed cells. Ligands of PPARc are considered as potential anticancer drugs, so CLA was tested for its ability to induce PPARc expression in MCF-7 breast cancer cells. The effects of CLA and of a specific synthetic PPARc antagonist were evaluated on cell growth as well as on parameters responsible for cell growth regulation. We demonstrated here that CLA stimulated the expression of PPARc to levels up to control and caused PPARc translocation into the nucleus. Furthermore, the overexpression of PPARc positively correlates with the inhibition of cell proliferation and with the modulation of ERK signaling induced by CLA; in all cases the administration of the antagonist reverted CLA effects. The PPAR-signaling pathway is connected with the b-catenin/Ecadherin pathway, thus we evaluated CLA effects on the expression and cellular distribution of these proteins, which are involved in cell adhesion and responsible for invasive behavior. The treatment with CLA determined the up-regulation and the redistribution of b-catenin and E-cadherin and the antagonist reverted only the effect on b-catenin. These studies indicate that CLA regulates PPARc expression by selectively acting as an agonist and may influence cell-cell adhesion and invasiveness of MCF-7 cells. ' 2007 Wiley-Liss, Inc.

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An overview of the effect of linoleic and conjugated‐linoleic acids on the growth of several human tumor cell lines

Cited by 110 publications

References 42 publications

Chemical composition and antioxidant activity of beebread, and its influence on the glioblastoma cell line (U87MG)

Chemical composition and antioxidant activity of beebread, and its influence on the glioblastoma cell line (U87MG)

PPARα agonist fenofibrate suppresses tumor growth through direct and indirect angiogenesis inhibition

Involvement of PPARγ and E‐cadherin/β‐catenin pathway in the antiproliferative effect of conjugated linoleic acid in MCF‐7 cells

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