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Progesterone receptor isoforms PRA and PRB differentially contribute to breast cancer cell migration through interaction with focal adhesion kinase complexes.

Bellance C, Khan JA, Meduri G, Guiochon-Mantel A, Lombès M, Loosfelt H.

Mol Biol Cell. 2013 May;24(9):1363-74. doi: 10.1091/mbc.E12-11-0807. Epub 2013 Mar 13.


p38 and p42/44 MAPKs differentially regulate progesterone receptor A and B isoform stabilization.

Khan JA, Amazit L, Bellance C, Guiochon-Mantel A, Lombès M, Loosfelt H.

Mol Endocrinol. 2011 Oct;25(10):1710-24. doi: 10.1210/me.2011-1042. Epub 2011 Aug 4.


Differential regulation of breast cancer-associated genes by progesterone receptor isoforms PRA and PRB in a new bi-inducible breast cancer cell line.

Khan JA, Bellance C, Guiochon-Mantel A, Lombès M, Loosfelt H.

PLoS One. 2012;7(9):e45993. doi: 10.1371/journal.pone.0045993. Epub 2012 Sep 24.


Altered progesterone receptor isoform expression remodels progestin responsiveness of breast cancer cells.

Graham JD, Yager ML, Hill HD, Byth K, O'Neill GM, Clarke CL.

Mol Endocrinol. 2005 Nov;19(11):2713-35. Epub 2005 Jun 23.


Progesterone receptor (PR) isoforms PRA and PRB differentially regulate expression of the breast cancer resistance protein in human placental choriocarcinoma BeWo cells.

Wang H, Lee EW, Zhou L, Leung PC, Ross DD, Unadkat JD, Mao Q.

Mol Pharmacol. 2008 Mar;73(3):845-54. Epub 2007 Nov 27.


A new class of orthosteric uPAR·uPA small-molecule antagonists are allosteric inhibitors of the uPAR·vitronectin interaction.

Liu D, Zhou D, Wang B, Knabe WE, Meroueh SO.

ACS Chem Biol. 2015 Jun 19;10(6):1521-34. doi: 10.1021/cb500832q. Epub 2015 Mar 31.


Progesterone Receptor Isoform Ratio: A Breast Cancer Prognostic and Predictive Factor for Antiprogestin Responsiveness.

Rojas PA, May M, Sequeira GR, Elia A, Alvarez M, Martínez P, Gonzalez P, Hewitt S, He X, Perou CM, Molinolo A, Gibbons L, Abba MC, Gass H, Lanari C.

J Natl Cancer Inst. 2017 Jul 1;109(7). doi: 10.1093/jnci/djw317.


Suppression of uPAR retards radiation-induced invasion and migration mediated by integrin β1/FAK signaling in medulloblastoma.

Nalla AK, Asuthkar S, Bhoopathi P, Gujrati M, Dinh DH, Rao JS.

PLoS One. 2010 Sep 24;5(9):e13006. doi: 10.1371/journal.pone.0013006.


Calcitonin inhibits invasion of breast cancer cells: involvement of urokinase-type plasminogen activator (uPA) and uPA receptor.

Han B, Nakamura M, Zhou G, Ishii A, Nakamura A, Bai Y, Mori I, Kakudo K.

Int J Oncol. 2006 Apr;28(4):807-14.


The urokinase-system in tumor tissue stroma of the breast and breast cancer cell invasion.

Hildenbrand R, Schaaf A.

Int J Oncol. 2009 Jan;34(1):15-23.


Ulipristal Acetate Inhibits Progesterone Receptor Isoform A-Mediated Human Breast Cancer Proliferation and BCl2-L1 Expression.

Esber N, Le Billan F, Resche-Rigon M, Loosfelt H, Lombès M, Chabbert-Buffet N.

PLoS One. 2015 Oct 16;10(10):e0140795. doi: 10.1371/journal.pone.0140795. eCollection 2015.


Progestin and antiprogestin responsiveness in breast cancer is driven by the PRA/PRB ratio via AIB1 or SMRT recruitment to the CCND1 and MYC promoters.

Wargon V, Riggio M, Giulianelli S, Sequeira GR, Rojas P, May M, Polo ML, Gorostiaga MA, Jacobsen B, Molinolo A, Novaro V, Lanari C.

Int J Cancer. 2015 Jun 1;136(11):2680-92. doi: 10.1002/ijc.29304. Epub 2014 Nov 12.


Subnuclear distribution of progesterone receptors A and B in normal and malignant endometrium.

Arnett-Mansfield RL, DeFazio A, Mote PA, Clarke CL.

J Clin Endocrinol Metab. 2004 Mar;89(3):1429-42.


Loss of co-ordinate expression of progesterone receptors A and B is an early event in breast carcinogenesis.

Mote PA, Bartow S, Tran N, Clarke CL.

Breast Cancer Res Treat. 2002 Mar;72(2):163-72.


Angiogenin interacts with the plasminogen activation system at the cell surface of breast cancer cells to regulate plasmin formation and cell migration.

Dutta S, Bandyopadhyay C, Bottero V, Veettil MV, Wilson L, Pins MR, Johnson KE, Warshall C, Chandran B.

Mol Oncol. 2014 May;8(3):483-507. doi: 10.1016/j.molonc.2013.12.017. Epub 2014 Jan 4.


Progestin effects on breast cancer cell proliferation, proteases activation, and in vivo development of metastatic phenotype all depend on progesterone receptor capacity to activate cytoplasmic signaling pathways.

Carnevale RP, Proietti CJ, Salatino M, Urtreger A, Peluffo G, Edwards DP, Boonyaratanakornkit V, Charreau EH, Bal de Kier Joffé E, Schillaci R, Elizalde PV.

Mol Endocrinol. 2007 Jun;21(6):1335-58. Epub 2007 Apr 17.


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