Interaction between FGFR-2, STAT5, and Progesterone Receptors in Breast Cancer

Cerliani, Juan P.; Guillardoy, Tomás; Giulianelli, Sebastián; Vaqué, José P.; Gutkind, J. Silvio; Vanzulli, Silvia I.; Martins, Rubén; Zeitlin, Eduardo; Lamb, Caroline A.; Lanari, Claudia

doi:10.1158/0008-5472.can-10-3074

Cited by 78 publications

(88 citation statements)

References 50 publications

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“…Frozen tumor sections were fixed in formalin, postfixed in 70% ethanol, blocked, and incubated with the primary antibodies and fluorescein isothiocyanate/TX-conjugated secondary antibodies, and counterstained with DAPI as described previously (18). Images were obtained using a Nikon Eclipse E800 Confocal Microscope and Nikon DS-U1 with ACT-2U software.…”

Section: Immunofluorescence and Colocalizationmentioning

confidence: 99%

“…Cultures growing on chamber slides were fixed in 70% ethanol and processed as described previously (18). To quantify nuclear colocalization of PR and ERa, we used the Pearson's correlation coefficient (R r ).…”

Section: Immunofluorescence and Colocalizationmentioning

confidence: 99%

“…Nuclear extracts containing 0.5 to 1 mg of proteins were subjected to immunoprecipitation (IP) using 2 mg of PR or ERa antibodies and rocked overnight at 4 C. The immunocomplexes were then captured by adding protein A-agarose (Santa Cruz) processed as described (18) and subjected to Western blots.…”

Section: Immunoprecipitation Assaysmentioning

confidence: 99%

“…Total RNA was isolated from cultures with TRIzol Reagent (Invitrogen) and converted to cDNA as described previously (18). Specific oligos for human MYC (NM_002467.4) and CCND1 (NM_053056.2) were designed using Primer-Blast (NCBI; Supplementary Table S1).…”

Section: Rna Preparation and Real-time Quantitative Pcrmentioning

confidence: 99%

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Estrogen Receptor Alpha Mediates Progestin-Induced Mammary Tumor Growth by Interacting with Progesterone Receptors at the Cyclin D1/MYC Promoters

et al. 2012

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Synthetic progesterone used in contraception drugs (progestins) can promote breast cancer growth, but the mechanisms involved are unknown. Moreover, it remains unclear whether cytoplasmic interactions between the progesterone receptor (PR) and estrogen receptor alpha (ERa) are required for PR activation. In this study, we used a murine progestin-dependent tumor to investigate the role of ERa in progestin-induced tumor cell proliferation. We found that treatment with the progestin medroxyprogesterone acetate (MPA) induced the expression and activation of ERa, as well as rapid nuclear colocalization of activated ERa with PR. Treatment with the pure antiestrogen fulvestrant to block ERa disrupted the interaction of ERa and PR in vitro and induced the regression of MPA-dependent tumor growth in vivo. ERa blockade also prevented an MPA-induced increase in CYCLIN D1 (CCND1) and MYC expression. Chromatin immunoprecipitation studies showed that MPA triggered binding of ERa and PR to the CCND1 and MYC promoters. Interestingly, blockade or RNAi-mediated silencing of ERa inhibited ERa, but not PR binding to both regulatory sequences, indicating that an interaction between ERa and PR at these sites is necessary for MPA-induced gene expression and cell proliferation. We confirmed that nuclear colocalization of both receptors also occurred in human breast cancer samples. Together, our findings argued that ERa-PR association on target gene promoters is essential for progestin-induced cell proliferation. Cancer Res; 72(9); 2416-27. Ó2012 AACR.

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Section: Immunofluorescence and Colocalizationmentioning

confidence: 99%

Section: Immunofluorescence and Colocalizationmentioning

confidence: 99%

Section: Immunoprecipitation Assaysmentioning

confidence: 99%

Section: Rna Preparation and Real-time Quantitative Pcrmentioning

confidence: 99%

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Estrogen Receptor Alpha Mediates Progestin-Induced Mammary Tumor Growth by Interacting with Progesterone Receptors at the Cyclin D1/MYC Promoters

et al. 2012

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“…This may partly explain the rapid rise of this disease here. The association of reproductive history and breast cancer might be understood from hormone target theory (Adami et al, 1995;Adami et al, 1998;Cerliani et al, 2011;Trepp et al, 2010). Mammary gland formation consists of three stages: organogenesis, which grows from terminal end bud (TEB) to non-pregnant primary ductal system with cuboidal epithelial cells and is stimulated by prolactin; mature gland formation, with highly branched ducts and lobular buds; pregnancy gland formation, through the stimulation of several hormones with differentiation of lobular buds into fully differentiated type III lobules with milk secreting columnal cells.…”

mentioning

confidence: 99%

Comparison of Genome Aberrations Between Early-Onset and Late-Onset Breast Cancer

Hsu¹,

Cheng²,

Chian-Feng³

et al. 2011

Breast Cancer - Recent Advances in Biology, Imaging and Therapeutics

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FGF7–FGFR2 autocrine signaling increases growth and chemoresistance of fusion‐positive rhabdomyosarcomas

et al. 2021

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Rhabdomyosarcomas are aggressive pediatric soft‐tissue sarcomas and include high‐risk PAX3–FOXO1 fusion‐gene‐positive cases. Fibroblast growth factor receptor 4 (FGFR4) is known to contribute to rhabdomyosarcoma progression; here, we sought to investigate the involvement and potential for therapeutic targeting of other FGFRs in this disease. Cell‐based screening of FGFR inhibitors with potential for clinical repurposing (NVP‐BGJ398, nintedanib, dovitinib, and ponatinib) revealed greater sensitivity of fusion‐gene‐positive versus fusion‐gene‐negative rhabdomyosarcoma cell lines and was shown to be correlated with high expression of FGFR2 and its specific ligand, FGF7. Furthermore, patient samples exhibit higher mRNA levels of FGFR2 and FGF7 in fusion‐gene‐positive versus fusion‐gene‐negative rhabdomyosarcomas. Sustained intracellular mitogen‐activated protein kinase (MAPK) activity and FGF7 secretion into culture media during serum starvation of PAX3–FOXO1 rhabdomyosarcoma cells together with decreased cell viability after genetic silencing of FGFR2 or FGF7 was in keeping with a novel FGF7–FGFR2 autocrine loop. FGFR inhibition with NVP‐BGJ398 reduced viability and was synergistic with SN38, the active metabolite of irinotecan. In vivo , NVP‐BGJ398 abrogated xenograft growth and warrants further investigation in combination with irinotecan as a therapeutic strategy for fusion‐gene‐positive rhabdomyosarcomas.

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Interaction between FGFR-2, STAT5, and Progesterone Receptors in Breast Cancer

Cited by 78 publications

References 50 publications

Estrogen Receptor Alpha Mediates Progestin-Induced Mammary Tumor Growth by Interacting with Progesterone Receptors at the Cyclin D1/MYC Promoters

Estrogen Receptor Alpha Mediates Progestin-Induced Mammary Tumor Growth by Interacting with Progesterone Receptors at the Cyclin D1/MYC Promoters

Comparison of Genome Aberrations Between Early-Onset and Late-Onset Breast Cancer

FGF7–FGFR2 autocrine signaling increases growth and chemoresistance of fusion‐positive rhabdomyosarcomas

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