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Chemical Compound Review

AGN-PC-00HRQ4     (17-ethanoyl-6,10,13- trimethyl-3-oxo-2,6,7...

Synonyms: SureCN14262777, AC1L1HA8, A19457, I06-0138, 1172-82-3, ...
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Disease relevance of Medroxyprogesterone acetate


Psychiatry related information on Medroxyprogesterone acetate

  • Medroxyprogesterone acetate (MPA) treatment of sexual acting out in men suffering from dementia [6].
  • All these groups also received 2.5 mg of medroxyprogesterone acetate (MPA) sequentially for the last 12 days of HRT, while the fourth therapy group received 0.625 mg/d of CEE and 2.5 mg/d of MPA continuously (n = 19) [7].
  • A case history was presented of a young man with mild mental retardation who was successfully treated with MPA [8].

High impact information on Medroxyprogesterone acetate

  • Treatment of C4HD cells with MPA induced Stat3 binding to DNA [9].
  • While expression of Stat3Y705-F mutant had an inhibitory effect on MPA-induced growth of C4HD cells, transfection with the constitutively activated Stat3-C vector resulted in MPA-independent proliferation [9].
  • In vitro, MC4-L2 and MC7-L1 were stimulated by MPA (nM to microM) and 17beta-estradiol (nM and 10 nM); no significant stimulation was observed in MC4-L1, MC4-L3, and MC4-L5 under the same experimental conditions [3].
  • When the cells were removed from MPA, TGF-alpha expression declined gradually, but EGF-receptor mRNA levels increased, as did EGF-binding activity [10].
  • MPA had no effect on TGF-alpha expression by HEC-50 cells [2].

Chemical compound and disease context of Medroxyprogesterone acetate


Biological context of Medroxyprogesterone acetate

  • To investigate the correlation between MPA-induced Stat3 activation and cell growth, C4HD cells were transiently transfected with a DN Stat3 expression vector, Stat3Y705-F, or with a constitutively activated Stat3 mutant, Stat3-C [9].
  • In addition, MPA induced rapid, nongenomic Stat3, Jak1, and Jak2 tyrosine phosphorylation in C4HD and T47D cells [9].
  • Incubation of both cell lines with MPA resulted in a time- and dose-dependent inhibition of cell proliferation [2].
  • Conversely, silencing of FOXO1 expression completely abolishes cell death induced by MPA withdrawal [15].
  • However, MPA treatment of T-47D cells resulted in a 55% decrease in overall AP-1 activity, as measured by transient transfection of an AP-1-regulated chloramphenicol acetyltransferase reporter gene [16].

Anatomical context of Medroxyprogesterone acetate

  • We found that C4HD epithelial cells, from the MPA-induced mammary tumor model, expressed Stat3 and that MPA treatment of C4HD cells up-regulated Stat3 protein expression [9].
  • Treatment with conjugated equine estrogens, but not MPA, augmented endothelium-mediated dilation of atherosclerotic coronary arteries [17].
  • Although no hybridized band was found in the proliferative and secretory phase endometria, a specific band of 5 kilobases, in agreement with the size of human prepro-EGF messenger ribonucleic acid, was detected in decidua of early pregnancy as well as in in vitro MPA-induced decidual cells [4].
  • In the cultured stromal cells, Northern analysis revealed a 4-fold increase in steady state levels of PAI-1 mRNA in response to 10(-6)-10(-8) mol/L MPA [18].
  • Medroxyprogesterone acetate (MPA) in advanced granulosa cell tumours of the ovary--a new therapeutic approach [19]?

Associations of Medroxyprogesterone acetate with other chemical compounds

  • A significant decrease in TGF-alpha mRNA was apparent 6 h after exposure to MPA and a further decrease was seen 12-24 h after addition of the progestin [2].
  • Our results also demonstrated that induction of steady state TF mRNA by MPA was abolished by treating cells with E2 plus MPA in conjunction with the protein synthesis inhibitor cycloheximide [20].
  • Polyacrylamide gel electrophoretic separation after immunoprecipitation of biosynthetically labeled PAs revealed that medroxyprogesterone acetate (MPA) lowered levels of secreted tissue type PA (tPA) at 67 kilodaltons and urokinase type PA (uPA) at 55 kilodaltons [21].
  • LDL was isolated from monkeys fed an atherogenic diet for 12 weeks or the same diet with CEE, MPA, CEE + MPA, or tamoxifen added at levels equivalent (on a caloric basis) to those given to women [22].
  • In these last lines the synthetic glucocorticoid, dexamethasone, was a more potent inducer of EGF binding than MPA, a known glucocorticoid agonist, while the high-affinity PR ligand, ORG 2058, was without effect [23].

Gene context of Medroxyprogesterone acetate

  • Recent data suggest that the presence of structurally altered AR in breast cancers may account for unresponsiveness to MPA in some of these cases [24].
  • VEGF production was also significantly greater in cells treated with db-cAMP (0.5 mmol/L) and MPA (1 nmol/L or 100 nmol/L) than in control cells [25].
  • HRG induced a potent proliferative effect on these cells and potentiated MPA mitogenic effects [26].
  • The level of TGF beta 3 mRNA in endometrial stromal cells, however, was decreased by MPA treatment [27].
  • Treatment of stromal cells with medroxyprogesterone acetate (MPA, a synthetic progestin) also effected a small increase in the level of TGF beta 1 mRNA [27].

Analytical, diagnostic and therapeutic context of Medroxyprogesterone acetate


  1. Quantitation of G0 and G1 phase cells in primary carcinomas. Antibody to M1 subunit of ribonucleotide reductase shows G1 phase restriction point block. Tay, D.L., Bhathal, P.S., Fox, R.M. J. Clin. Invest. (1991) [Pubmed]
  2. Transforming growth factor gene expression in human endometrial adenocarcinoma cells: regulation by progestins. Gong, Y., Anzai, Y., Murphy, L.C., Ballejo, G., Holinka, C.F., Gurpide, E., Murphy, L.J. Cancer Res. (1991) [Pubmed]
  3. Five novel hormone-responsive cell lines derived from murine mammary ductal carcinomas: in vivo and in vitro effects of estrogens and progestins. Lanari, C., Lüthy, I., Lamb, C.A., Fabris, V., Pagano, E., Helguero, L.A., Sanjuan, N., Merani, S., Molinolo, A.A. Cancer Res. (2001) [Pubmed]
  4. Gene expression of epidermal growth factor in human endometrium during decidualization. Sakakibara, H., Taga, M., Saji, M., Kida, H., Minaguchi, H. J. Clin. Endocrinol. Metab. (1994) [Pubmed]
  5. Long-term progestin treatment inhibits RANTES (regulated on activation, normal T cell expressed and secreted) gene expression in human endometrial stromal cells. Zhao, D., Lebovic, D.I., Taylor, R.N. J. Clin. Endocrinol. Metab. (2002) [Pubmed]
  6. Medroxyprogesterone acetate (MPA) treatment of sexual acting out in men suffering from dementia. Cooper, A.J. The Journal of clinical psychiatry. (1987) [Pubmed]
  7. Circulating hormone levels in menopausal women receiving different hormone replacement therapy regimens. A comparison. Castelo-Branco, C., Martínez de Osaba, M.J., Fortuny, A., Iglesias, X., González-Merlo, J. The Journal of reproductive medicine. (1995) [Pubmed]
  8. Treatment of sexual offenses by persons with developmental disabilities. Myers, B.A. American journal of mental retardation : AJMR. (1991) [Pubmed]
  9. Progestins induce transcriptional activation of signal transducer and activator of transcription 3 (Stat3) via a Jak- and Src-dependent mechanism in breast cancer cells. Proietti, C., Salatino, M., Rosemblit, C., Carnevale, R., Pecci, A., Kornblihtt, A.R., Molinolo, A.A., Frahm, I., Charreau, E.H., Schillaci, R., Elizalde, P.V. Mol. Cell. Biol. (2005) [Pubmed]
  10. Mechanisms involved in the evolution of progestin resistance in human breast cancer cells. Murphy, L.C., Dotzlaw, H., Wong, M.S., Miller, T., Murphy, L.J. Cancer Res. (1991) [Pubmed]
  11. A randomized comparison of megestrol acetate (MA) and medroxyprogesterone acetate (MPA) in patients with advanced breast cancer. Willemse, P.H., van der Ploeg, E., Sleijfer, D.T., Tjabbes, T., van Veelen, H. Eur. J. Cancer (1990) [Pubmed]
  12. Dose of progestin in postmenopausal-combined hormone therapy and risk of endometrial cancer. Reed, S.D., Voigt, L.F., Beresford, S.A., Hill, D.A., Doherty, J.A., Weiss, N.S. Am. J. Obstet. Gynecol. (2004) [Pubmed]
  13. Experiences with doxo/epirubicin and medroxyprogesterone acetate (MPA) in prostatic cancer. Anderström, C. Cancer Chemother. Pharmacol. (1994) [Pubmed]
  14. Hypoluteoidism in a bitch. Görlinger, S., Galac, S., Kooistra, H.S., Okkens, A.C. Theriogenology (2005) [Pubmed]
  15. Progestins regulate the expression and activity of the forkhead transcription factor FOXO1 in differentiating human endometrium. Labied, S., Kajihara, T., Madureira, P.A., Fusi, L., Jones, M.C., Higham, J.M., Varshochi, R., Francis, J.M., Zoumpoulidou, G., Essafi, A., Fernandez de Mattos, S., Lam, E.W., Brosens, J.J. Mol. Endocrinol. (2006) [Pubmed]
  16. Regulation of c-jun and jun-B by progestins in T-47D human breast cancer cells. Alkhalaf, M., Murphy, L.C. Mol. Endocrinol. (1992) [Pubmed]
  17. Effects of hormone replacement therapy on reactivity of atherosclerotic coronary arteries in cynomolgus monkeys. Williams, J.K., Honoré, E.K., Washburn, S.A., Clarkson, T.B. J. Am. Coll. Cardiol. (1994) [Pubmed]
  18. Progestin regulation of plasminogen activator inhibitor type 1 in primary cultures of endometrial stromal and decidual cells. Schatz, F., Lockwood, C.J. J. Clin. Endocrinol. Metab. (1993) [Pubmed]
  19. Medroxyprogesterone acetate (MPA) in advanced granulosa cell tumours of the ovary--a new therapeutic approach? Malik, S.T., Slevin, M.L. Br. J. Cancer (1991) [Pubmed]
  20. Transcriptional regulation of the tissue factor gene by progestins in human endometrial stromal cells. Krikun, G., Schatz, F., Mackman, N., Guller, S., Lockwood, C.J. J. Clin. Endocrinol. Metab. (1998) [Pubmed]
  21. Plasminogen activator activity during decidualization of human endometrial stromal cells is regulated by plasminogen activator inhibitor 1. Schatz, F., Aigner, S., Papp, C., Toth-Pal, E., Hausknecht, V., Lockwood, C.J. J. Clin. Endocrinol. Metab. (1995) [Pubmed]
  22. In vitro lipid peroxidation of LDL from postmenopausal cynomolgus macaques treated with female hormones. Schwenke, D.C., Wagner, J.D., Adams, M.R. J. Lipid Res. (1999) [Pubmed]
  23. Regulation of epidermal growth factor receptor by progestins and glucocorticoids in human breast cancer cell lines. Ewing, T.M., Murphy, L.J., Ng, M.L., Pang, G.Y., Lee, C.S., Watts, C.K., Sutherland, R.L. Int. J. Cancer (1989) [Pubmed]
  24. Role of the androgen receptor in human breast cancer. Birrell, S.N., Hall, R.E., Tilley, W.D. Journal of mammary gland biology and neoplasia. (1998) [Pubmed]
  25. Changes in vascular endothelial growth factor production associated with decidualization by human endometrial stromal cells in vitro. Matsui, N., Kawano, Y., Nakamura, S., Miyakawa, I. Acta obstetricia et gynecologica Scandinavica. (2004) [Pubmed]
  26. Interactions between progestins and heregulin (HRG) signaling pathways: HRG acts as mediator of progestins proliferative effects in mouse mammary adenocarcinomas. Balañá, M.E., Lupu, R., Labriola, L., Charreau, E.H., Elizalde, P.V. Oncogene (1999) [Pubmed]
  27. Modulation of the levels of transforming growth factor beta messenger ribonucleic acids in human endometrial stromal cells. Arici, A., MacDonald, P.C., Casey, M.L. Biol. Reprod. (1996) [Pubmed]
  28. Activation of ErbB-2 via a hierarchical interaction between ErbB-2 and type I insulin-like growth factor receptor in mammary tumor cells. Balañá, M.E., Labriola, L., Salatino, M., Movsichoff, F., Peters, G., Charreau, E.H., Elizalde, P.V. Oncogene (2001) [Pubmed]
  29. Expression of 11 beta-hydroxysteroid dehydrogenase during decidualization of human endometrial stromal cells. Arcuri, F., Monder, C., Lockwood, C.J., Schatz, F. Endocrinology (1996) [Pubmed]
  30. Effects of postmenopausal hormone therapy every day and every other day on lipid levels according to difference in body mass index. Yasui, T., Umino, Y., Takikawa, M., Uemura, H., Kuwahara, A., Matsuzaki, T., Maegawa, M., Furumoto, H., Miura, M., Irahara, M. Menopause (New York, N.Y.) (2005) [Pubmed]
  31. Sequential hormonal therapy and sequential hormonal and chemotherapy for advanced prostatic cancer. Ruff, P., Derman, D.P., Weaving, A., Bezwoda, W.R. Oncology (1989) [Pubmed]
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