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Receptor activator for nuclear factor-κB ligand signaling promotes progesterone-mediated estrogen-induced mammary carcinogenesis.

Boopalan T, Arumugam A, Parada J, Saltzstein E, Lakshmanaswamy R - Cancer Sci. (2015)

Bottom Line: In ACI rats, mifepristone significantly reduced the incidence of mammary tumors.Likewise, mifepristone also inhibited the proliferation of MCF-7 cells.Mechanistic studies in MCF-7 cells reveal that RANKL induced upstream stimulatory factor-1 and NF-κB, resulting in subsequent activation of their downstream target GLI-1.

View Article: PubMed Central - PubMed

Affiliation: Center of Excellence in Cancer Research, Texas Tech University Health Sciences Center, El Paso, Texas, USA.

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Effects of hormones on cell proliferation. Cell proliferation of (a) MCF-7 cells (b) rat primary epithelial cells treated with estradiol (E), progesterone (P), or mifepristone (M) alone or in combination for 24 h. Data represent the mean ± SEM (n = 6). *P < 0.05 when compared with control (CON). NS, non-significant when compared with control.
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fig02: Effects of hormones on cell proliferation. Cell proliferation of (a) MCF-7 cells (b) rat primary epithelial cells treated with estradiol (E), progesterone (P), or mifepristone (M) alone or in combination for 24 h. Data represent the mean ± SEM (n = 6). *P < 0.05 when compared with control (CON). NS, non-significant when compared with control.

Mentions: We measured cell proliferation using the MTS assay.22 Estradiol alone, progesterone alone, and the combination of estradiol and progesterone increased the proliferation of MCF-7 cells by 23.6%, 21.8%, and 35.2%, respectively (Fig.2a). Similarly, estradiol alone, progesterone alone, and the combination of estradiol and progesterone increased the proliferation of rat primary mammary epithelial cells by 61%, 57%, and 69.7%, respectively (Fig.2b). The combination of estradiol and mifepristone inhibited the proliferation of MCF-7 cells and rat primary mammary-epithelial cells by 17.2% and 16.3%, respectively, when compared with the estradiol alone treated group.


Receptor activator for nuclear factor-κB ligand signaling promotes progesterone-mediated estrogen-induced mammary carcinogenesis.

Boopalan T, Arumugam A, Parada J, Saltzstein E, Lakshmanaswamy R - Cancer Sci. (2015)

Effects of hormones on cell proliferation. Cell proliferation of (a) MCF-7 cells (b) rat primary epithelial cells treated with estradiol (E), progesterone (P), or mifepristone (M) alone or in combination for 24 h. Data represent the mean ± SEM (n = 6). *P < 0.05 when compared with control (CON). NS, non-significant when compared with control.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4317778&req=5

fig02: Effects of hormones on cell proliferation. Cell proliferation of (a) MCF-7 cells (b) rat primary epithelial cells treated with estradiol (E), progesterone (P), or mifepristone (M) alone or in combination for 24 h. Data represent the mean ± SEM (n = 6). *P < 0.05 when compared with control (CON). NS, non-significant when compared with control.
Mentions: We measured cell proliferation using the MTS assay.22 Estradiol alone, progesterone alone, and the combination of estradiol and progesterone increased the proliferation of MCF-7 cells by 23.6%, 21.8%, and 35.2%, respectively (Fig.2a). Similarly, estradiol alone, progesterone alone, and the combination of estradiol and progesterone increased the proliferation of rat primary mammary epithelial cells by 61%, 57%, and 69.7%, respectively (Fig.2b). The combination of estradiol and mifepristone inhibited the proliferation of MCF-7 cells and rat primary mammary-epithelial cells by 17.2% and 16.3%, respectively, when compared with the estradiol alone treated group.

Bottom Line: In ACI rats, mifepristone significantly reduced the incidence of mammary tumors.Likewise, mifepristone also inhibited the proliferation of MCF-7 cells.Mechanistic studies in MCF-7 cells reveal that RANKL induced upstream stimulatory factor-1 and NF-κB, resulting in subsequent activation of their downstream target GLI-1.

View Article: PubMed Central - PubMed

Affiliation: Center of Excellence in Cancer Research, Texas Tech University Health Sciences Center, El Paso, Texas, USA.

Show MeSH
Related in: MedlinePlus