Modulation of membrane fluidity and lipidic metabolism in transformed rat fibroblasts induced by the sesquiterpenic hormone farnesylacetone

Rodes, Jean-François; Berreur-Bonnenfant, J.; Trémolières, A.; Brown, Spencer

doi:10.1002/cyto.990190305

Cited by 15 publications

(11 citation statements)

References 35 publications

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“…On day 6 following treatment, the cells were collected by trypsinization, washed with PBS, and stained with 100 ng/ml Nile red fluorescent dye (Sigma-Aldrich) in PBS for 5 minutes at room temperature. The stained cells were then washed twice with PBS, resuspended in PBS, and analyzed by flow cytometry [55]. …”

Section: Methodsmentioning

confidence: 99%

Anti-tumor effects of retinoids combined with trastuzumab or tamoxifen in breast cancer cells: induction of apoptosis by retinoid/trastuzumab combinations

et al. 2010

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IntroductionHER2 and estrogen receptor (ER) are important in breast cancer and are therapeutic targets of trastuzumab (Herceptin) and tamoxifen, respectively. Retinoids inhibit breast cancer growth, and modulate signaling by HER2 and ER. We hypothesized that treatment with retinoids and simultaneous targeting of HER2 and/or ER may have enhanced anti-tumor effects.MethodsThe effects of retinoids combined with trastuzumab or tamoxifen were examined in two human breast cancer cell lines in culture, BT474 and SKBR3. Assays of proliferation, apoptosis, differentiation, cell cycle distribution, and receptor signaling were performed.ResultsIn HER2-overexpressing/ER-positive BT474 cells, combining all-trans retinoic acid (atRA) with tamoxifen or trastuzumab synergistically inhibited cell growth, and altered cell differentiation and cell cycle. Only atRA/trastuzumab-containing combinations induced apoptosis. BT474 and HER2-overexpressing/ER-negative SKBR3 cells were treated with a panel of retinoids (atRA, 9-cis-retinoic acid, 13-cis-retinoic acid, or N-(4-hydroxyphenyl) retinamide (fenretinide) (4-HPR)) combined with trastuzumab. In BT474 cells, none of the single agents except 4-HPR induced apoptosis, but again combinations of each retinoid with trastuzumab did induce apoptosis. In contrast, the single retinoid agents did cause apoptosis in SKBR3 cells; this was only modestly enhanced by addition of trastuzumab. The retinoid drug combinations altered signaling by HER2 and ER. Retinoids were inactive in trastuzumab-resistant BT474 cells.ConclusionsCombining retinoids with trastuzumab maximally inhibits cell growth and induces apoptosis in trastuzumab-sensitive cells. Treatment with such combinations may have benefit for breast cancer patients.

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Section: Methodsmentioning

confidence: 99%

Anti-tumor effects of retinoids combined with trastuzumab or tamoxifen in breast cancer cells: induction of apoptosis by retinoid/trastuzumab combinations

et al. 2010

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“…After thorough rinsing in distilled water, slides were mounted in Aquamount for direct microscopic visualization of red-staining lipid droplets. Alternatively, staining of neutral lipid droplets in the cellular cytoplasm was done as described previously (40). In brief, the cells suspended in phosphate-buffered saline (10 6 cells/ml) were incubated for 5 min with Nile red (final concentration, 100 ng/ml) at room temperature.…”

Section: Fig 1 (A)mentioning

confidence: 99%

HER4 Mediates Ligand-Dependent Antiproliferative and Differentiation Responses in Human Breast Cancer Cells

Sartor

Zhou

Kozłowska

et al. 2001

Molecular and Cellular Biology

165

155

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The function of the epidermal growth factor receptor (EGFR) family member HER4 remains unclear because its activating ligand, heregulin, results in either proliferation or differentiation. This variable response may stem from the range of signals generated by HER4 homodimers versus heterodimeric complexes with other EGFR family members. The ratio of homo-and heterodimeric complexes may be influenced both by a cell's EGFR family member expression profile and by the ligand or even ligand isoform used. To define the role of HER4 in mediating antiproliferative and differentiation responses, human breast cancer cell lines were screened for responses to heregulin. Only cells that expressed HER4 exhibited heregulin-dependent antiproliferative responses. In-depth studies of one line, SUM44, demonstrated that the antiproliferative and differentiation responses correlated with HER4 activation and were abolished by stable expression of a kinase-inactive HER4. HB-EGF, a HER4-specific ligand in this EGFR-negative cell line, also induced an antiproliferative response. Moreover, introduction and stable expression of HER4 in HER4-negative SUM102 cells resulted in the acquisition of a heregulin-dependent antiproliferative response, associated with increases in markers of differentiation. The role of HER2 in these heregulin-dependent responses was examined through elimination of cell surface HER2 signaling by stable expression of a single-chain anti-HER2 antibody that sequestered HER2 in the endoplasmic reticulum. In the cell lines with either endogenously (SUM44) or exogenously (SUM102) expressed HER4, elimination of HER2 did not alter HER4-dependent decreases in cell growth. These results suggest that HER4 is both necessary and sufficient to trigger an antiproliferative response in human breast cancer cells.The epidermal growth factor receptor (EGFR) family has been implicated in breast cancer pathogenesis and progression (reviewed in references 13 and 39). Aberrant expression of at least two of the family members, EGFR and HER2, has been associated with poor prognosis and differential response to therapy (21,28,31,44). Recently, treatment targeted against HER2 has demonstrated clinical efficacy, emphasizing the importance of members of this receptor family in breast cancer prognosis and therapy (10).The EGFR family consists of four known members: EGFR (HER1, erbB-1), HER2 (erbB-2), HER3 (erbB-3), and HER4 (erbB-4) (reviewed in references 13, 34, and 39). The four receptors form homodimers or heterodimers upon activation by two sets of ligands, the EGF and heregulin/neuregulin families. There are several possible hetero-and homodimeric receptor combinations, which theoretically result in differential activation of multiple downstream signal transduction pathways. Additional heterogeneity results from varying phenotypic responses, depending on cell type and the duration or intensity of downstream signaling, determined in part by differences in ligand affinity, recycling, and intracellular environment, as well as other factors th...

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“…The argon laser (SpectraPhysics 2025-05) with vertically polarized output was set at 351-364 nm and 50 mW. The signals were processed on an analog card linked to a 1,024-channel ADC to derive the blue emission anisotropy (r) as described by Rodes et al (1994). The forward-angle light scatter (FALS) was used to gate the analysis upon intact cells.…”

Section: Treatment Of Cells For Flow Cytometrymentioning

confidence: 99%

“…These drops also could have modified the refringence of the cytoplasm and contributed to the increase in FALS. Such drops are considered a sign of toxicity in rat fibroblast cells (Rodes et al 1994). …”

Section: Effect Of Pr On Lipid Metabolismmentioning

confidence: 99%

Biochemical alterations in paromomycin-treated Leishmania donovani promastigotes

Maarouf

Lawrence

Brown

et al. 1997

Parasitology Research

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Paromomycin is used for the treatment of leishmaniasis in humans, but little is known about its mechanism of action. Investigating the effect of this antibiotic on promastigotes of Leishmania donovani, we showed that inhibition of the multiplication of these parasites could be related to its effect on RNA synthesis and to modifications of membranous polar lipids and membrane fluidity, leading to altered membrane permeability.

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Modulation of membrane fluidity and lipidic metabolism in transformed rat fibroblasts induced by the sesquiterpenic hormone farnesylacetone

Cited by 15 publications

References 35 publications

Anti-tumor effects of retinoids combined with trastuzumab or tamoxifen in breast cancer cells: induction of apoptosis by retinoid/trastuzumab combinations

Anti-tumor effects of retinoids combined with trastuzumab or tamoxifen in breast cancer cells: induction of apoptosis by retinoid/trastuzumab combinations

HER4 Mediates Ligand-Dependent Antiproliferative and Differentiation Responses in Human Breast Cancer Cells

Biochemical alterations in paromomycin-treated Leishmania donovani promastigotes

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