Effects of TGF‐β1 (transforming growth factor‐β1) on the cell cycle regulation of human breast adenocarcinoma (MCF‐7) cells

Mazars, Philippe; Barboule, Nadia; Baldin, Véronique; Vidal, Simone; Ducommun, Bernard; Valette, Annie

doi:10.1016/0014-5793(95)00247-7

Cited by 41 publications

(24 citation statements)

References 28 publications

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“…In the present study, it was demonstrated that recombinant TGF-β inhibited the proliferation of MCF-7 cells. This result was consistent with a previous study by Mazars et al (22). Porcine TGF-β1 was used in the study by Mazars et al (22), whereas the present study used recombinant human TGF-β, which was more suitable for the physiological conditions.…”

Section: Ink4bsupporting

confidence: 93%

Rapamycin enhances the antiproliferative effect of transforming growth factor-β on MCF-7 human breast cancer cells

Wang

Yin

2017

Experimental and Therapeutic Medicine

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Abstract. Transforming growth factor-β (TGF-β), a well-known cytokine with pleiotropic biological functions, has an important role in the regulation of cellular proliferation. Rapamycin has specific antagonistic activity on the function of the mammalian target of the rapamycin signaling pathway. The cooperation of TGF-β and rapamycin on the proliferation of Michigan Cancer Foundation (MCF)-7 human breast cancer cells is unclear. The present study demonstrated that TGF-β had a growth-arresting effect on MCF-7 cancer cells. TGF-β stimulation resulted in the upregulation of several cyclin-dependent kinase inhibitors, including p14 ARF , p15 INK4b, p16INK4a and p21. The present study also demonstrated that rapamycin enhances the antiproliferative effect of TGF-β. The combination of rapamycin and TGF-β induced apoptosis of MCF-7 tumor cells. These findings advance the current understanding of the biological effects of TGF-β and rapamycin.

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Section: Ink4bsupporting

confidence: 93%

Rapamycin enhances the antiproliferative effect of transforming growth factor-β on MCF-7 human breast cancer cells

Wang

Yin

2017

Experimental and Therapeutic Medicine

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“…For example, lycopene like tamoxifen, pure antiestrogens, retinoids, progestins, TGF-b and TNF-a reduces cyclin D protein abundance (Jeoung et al, 1995;Mazars et al, 1995;Planas Silva and Weinberg, 1997;Watts et al, 1995). Whereas most of these agents have been shown to increase levels of the CDK inhibitors, p21 and p27, lycopene, like retinoic acid, reduces p21 levels.…”

Section: Discussionmentioning

confidence: 99%

“…Most interestingly, many anticancer agents, including those used for breast cancer therapy, convey their inhibitory e ect in G 1 phase primarily by reducing cyclin D1 levels. These include pure antiestrogens (Watts et al, 1994), tamoxifen (Planas Silva and Weinberg, 1997), retinoids (Teixeira and Pratt, 1997;Zhou et al, 1997), progestins (Musgrove et al, 1998), as well as 1.25-dihydroxyvitamin D 3 (Wang et al, 1996) and TGF-b (Mazars et al, 1995).…”

Section: Introductionmentioning

confidence: 99%

Lycopene inhibition of cell cycle progression in breast and endometrial cancer cells is associated with reduction in cyclin D levels and retention of p27Kip1 in the cyclin E–cdk2 complexes

et al. 2001

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Numerous studies have demonstrated the anticancer activity of the tomato carotenoid, lycopene. However, the molecular mechanism of this action remains unknown. Lycopene inhibition of human breast and endometrial cancer cell growth is associated with inhibition of cell cycle progression at the G 1 phase. In this study we determined the lycopene-mediated changes in the cell cycle machinery. Cells synchronized in the G 1 phase by serum deprivation were treated with lycopene or vehicle and restimulated with 5% serum. Lycopene treatment decreased serum-induced phosphorylation of the retinoblastoma protein and related pocket proteins. This e ect was associated with reduced cyclin-dependent kinase (cdk4 and cdk2) activities with no alterations in CDK protein levels. Lycopene caused a decrease in cyclin D1 and D3 levels whereas cyclin E levels did not change. The CDK inhibitor p21 Cip1/Waf1 abundance was reduced while p27 Kip1 levels were unaltered in comparison to control cells. Serum stimulation of control cells resulted in reduction in the p27 content in the cyclin E ± cdk2 complex and its accumulation in the cyclin D1 ± cdk4 complex. This change in distribution was largely prevented by lycopene treatment. These results suggest that lycopene inhibits cell cycle progression via reduction of the cyclin D level and retention of p27 in cyclin E ± cdk2, thus leading to inhibition of G 1 CDK activities. Oncogene (2001) 20, 3428 ± 3436.

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“…Transforming growth factor b (TGFb), a potent growth inhibitor for breast cancer cells, has been shown to directly enhance p21 expression via a TGFb responsive element in the p21 promoter (Datto et al, 1995). TGFb upregulated p21 in ovarian adenocarcinoma cells (Elbendary et al, 1994) and increased p21 nuclear localization in TGFb responsive human breast cancer MCF-7 cells in a TGFb type II receptor (RII) dependent manner (Mazars et al, 1995). TGFb receptors were found to be repressed in many malignancies including estrogen receptor positive breast cancer cell lines (Brattain et al, 1996;Kalkhoven et al, 1995) and reconstitution of a functional receptor system led to reduced malignancy (Sun et al, 1994).…”

Section: Discussionmentioning

confidence: 99%

Modulation of cell cycle control by vitamin D3 and its analogue, EB1089, in human breast cancer cells

Fan

et al. 1997

Oncogene

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Examination of a panel of ER positive breast cancer cell lines showed that they were dierentially growth inhibited by vitamin D 3 and its analogue EB1089. EB1089 treatment of the breast cancer cell lines MCF-7 E, BT20, T47D, and ZR75 demonstrated a correlation between a reduction in Cdk2 kinase activity towards phosphorylation of histone H1 and a decrease in DNA synthesis, while no modulation of Cdk2 activity was observed in the vitamin D 3 and EB1089 resistant cell line MCF-7 L. This was accompanied by a time dependent decrease in the percentage of S phase cells in the responsive lines. Characterization of the expression levels of Cdk2 and its related cell cycle proteins in MCF-7 E cells showed that after EB1089 treatment, there was a concentration and time dependent up-regulation of p21 as well as a decrease in cyclin A proteins. Paradoxically, cyclin E levels were increased as a function of treatment. Analysis of cyclin-Cdk2-Cdki complex formation showed that in EB1089 treated MCF-7 E cells, Cdk2, cyclin A and cyclin E immunoprecipitates contained an increased abundance of p21. In contrast to MCF-7 E cells, increases in both p21 and p27 as well as their complex formation with Cdk2 were observed in BT20 and ZR75 cells. These ®ndings indicate that up-regulation of p21 as well as p27 in some cell types may account for the inactivation of Cdk2 activity and a G 1 block of the cell cycle following EB1089 treatment.

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Effects of TGF‐β1 (transforming growth factor‐β1) on the cell cycle regulation of human breast adenocarcinoma (MCF‐7) cells

Cited by 41 publications

References 28 publications

Rapamycin enhances the antiproliferative effect of transforming growth factor-β on MCF-7 human breast cancer cells

Rapamycin enhances the antiproliferative effect of transforming growth factor-β on MCF-7 human breast cancer cells

Lycopene inhibition of cell cycle progression in breast and endometrial cancer cells is associated with reduction in cyclin D levels and retention of p27Kip1 in the cyclin E–cdk2 complexes

Modulation of cell cycle control by vitamin D3 and its analogue, EB1089, in human breast cancer cells

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