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RESEARCH ARTICLE

FOXM1 is lower in human fetal membranes after spontaneous preterm labour and delivery

Ratana Lim A B , Gillian Barker A B and Martha Lappas A B C
+ Author Affiliations
- Author Affiliations

A Department of Obstetrics and Gynaecology, University of Melbourne, Parkville, Vic. 3010, Australia.

B Mercy Perinatal Research Centre, Mercy Hospital for Women, 4th Floor, 163 Studley Road, Heidelberg, Vic. 3084, Australia.

C Corresponding author. Email: mlappas@unimelb.edu.au

Reproduction, Fertility and Development 26(7) 1052-1060 https://doi.org/10.1071/RD13140
Submitted: 7 May 2013  Accepted: 29 July 2013   Published: 19 August 2013

Abstract

Spontaneous preterm birth is usually associated with infection, inflammation or both. Forkhead box (FOX) M1 (FOXM1), a member of the FOX family of transcription factors, has been associated with inflammation. The aim of this study was to determine whether FOXM1 regulates the expression and release of pro-labour mediators in human gestational tissues. FOXM1 mRNA and protein expression were determined in fetal membranes from women at (1) preterm no labour: Caesarean section with no labour and (2) preterm labour: after spontaneous labour and delivery. Primary amnion cells were utilised to investigate the effect of small interfering RNA (siRNA)-mediated gene silencing of FOXM1 on pro-labour mediators. Spontaneous preterm labour decreased FOXM1 gene and nuclear protein expression. FOXM1 silencing in primary amnion cells increased interleukin (IL)-1β-induced pro-inflammatory cytokines (IL-6 and IL-8 mRNA expression and secretion), cyclooxygenase (COX)-2 expression and subsequent prostaglandin (PG)E2 and PGF release as well as gene expression and secretion of the matrix-degrading enzyme matrix metalloproteinase 9 (MMP-9). In conclusion, spontaneous preterm labour is associated with decreased FOXM1 expression in fetal membranes.

Additional keywords: cytokines, preterm labour, prostaglandins.


References

Ahmed, M., Uddin, S., Hussain, A. R., Alyan, A., Jehan, Z., Al-Dayel, F., Al-Nuaim, A., Al-Sobhi, S., Amin, T., Bavi, P., and Al-Kuraya, K. S. (2012). FoxM1 and its association with matrix metalloproteinases (MMP) signalling pathway in papillary thyroid carcinoma. J. Clin. Endocrinol. Metab. 97, E1–E13.
FoxM1 and its association with matrix metalloproteinases (MMP) signalling pathway in papillary thyroid carcinoma.Crossref | GoogleScholarGoogle Scholar | 1:CAS:528:DC%2BC38XhsVKqtL4%3D&md5=003890d93001f352c070a85d7bacd6e0CAS | 22049175PubMed |

Balli, D., Zhang, Y., Snyder, J., Kalinichenko, V. V., and Kalin, T. V. (2011). Endothelial cell-specific deletion of transcription factor FoxM1 increases urethane-induced lung carcinogenesis. Cancer Res. 71, 40–50.
Endothelial cell-specific deletion of transcription factor FoxM1 increases urethane-induced lung carcinogenesis.Crossref | GoogleScholarGoogle Scholar | 1:CAS:528:DC%2BC3MXovF2r&md5=1f8c1f709b019fc9d855a455960a015aCAS | 21199796PubMed |

Balli, D., Ren, X., Chou, F. S., Cross, E., Zhang, Y., Kalinichenko, V. V., and Kalin, T. V. (2012). Foxm1 transcription factor is required for macrophage migration during lung inflammation and tumour formation. Oncogene 31, 3875–3888.
Foxm1 transcription factor is required for macrophage migration during lung inflammation and tumour formation.Crossref | GoogleScholarGoogle Scholar | 1:CAS:528:DC%2BC3MXhsFKksrjL&md5=09744770cc5d933287c2880389feb712CAS | 22139074PubMed |

Beck, S., Wojdyla, D., Say, L., Betran, A. P., Merialdi, M., Requejo, J. H., Rubens, C., Menon, R., and Van Look, P. F. (2010). The worldwide incidence of preterm birth: a systematic review of maternal mortality and morbidity. Bull. World Health Organ. 88, 31–38.
The worldwide incidence of preterm birth: a systematic review of maternal mortality and morbidity.Crossref | GoogleScholarGoogle Scholar | 20428351PubMed |

Bhat, U. G., Halasi, M., and Gartel, A. L. (2009). FoxM1 is a general target for proteasome inhibitors. PLoS ONE 4, e6593.
| 19672316PubMed |

Bolt, R. J., van Weissenbruch, M. M., Lafeber, H. N., and Delemarre-van de Waal, H. A. (2001). Glucocorticoids and lung development in the fetus and preterm infant. Pediatr. Pulmonol. 32, 76–91.
Glucocorticoids and lung development in the fetus and preterm infant.Crossref | GoogleScholarGoogle Scholar | 1:STN:280:DC%2BD3Mzlt1aitA%3D%3D&md5=f540931891cd8f9fd3345ef172f2ca4bCAS | 11416880PubMed |

Christiaens, I., Zaragoza, D. B., Guilbert, L., Robertson, S. A., Mitchell, B. F., and Olson, D. M. (2008). Inflammatory processes in preterm and term parturition. J. Reprod. Immunol. 79, 50–57.
Inflammatory processes in preterm and term parturition.Crossref | GoogleScholarGoogle Scholar | 1:CAS:528:DC%2BD1cXht1eju7rE&md5=c22b35596eabd509856e9c9afbaa55ecCAS | 18550178PubMed |

Dammann, O., and Leviton, A. (1998). Infection remote from the brain, neonatal white matter damage and cerebral palsy in the preterm infant. Semin. Pediatr. Neurol. 5, 190–201.
Infection remote from the brain, neonatal white matter damage and cerebral palsy in the preterm infant.Crossref | GoogleScholarGoogle Scholar | 1:STN:280:DyaK1cvltVymsA%3D%3D&md5=ac4bef8e06826d54c348e7f3eeb46805CAS | 9777677PubMed |

Dammann, O., Kuban, K. C., and Leviton, A. (2002). Perinatal infection, fetal inflammatory response, white matter damage and cognitive limitations in children born preterm. Ment. Retard. Dev. Disabil. Res. Rev. 8, 46–50.
Perinatal infection, fetal inflammatory response, white matter damage and cognitive limitations in children born preterm.Crossref | GoogleScholarGoogle Scholar | 11921386PubMed |

Fortunato, S. J., Menon, R., and Lombardi, S. J. (1999). MMP/TIMP imbalance in amniotic fluid during PROM: an indirect support for endogenous pathway to membrane rupture. J. Perinat. Med. 27, 362–368.
MMP/TIMP imbalance in amniotic fluid during PROM: an indirect support for endogenous pathway to membrane rupture.Crossref | GoogleScholarGoogle Scholar | 1:CAS:528:DyaK1MXnvFKgs78%3D&md5=2de8742ba6f2a7296e3284816d7be3ffCAS | 10642956PubMed |

Fortunato, S. J., Menon, R., Bryant, C., and Lombardi, S. J. (2000). Programmed cell death (apoptosis) as a possible pathway to metalloproteinase activation and fetal membrane degradation in premature rupture of membranes. Am. J. Obstet. Gynecol. 182, 1468–1476.
Programmed cell death (apoptosis) as a possible pathway to metalloproteinase activation and fetal membrane degradation in premature rupture of membranes.Crossref | GoogleScholarGoogle Scholar | 1:CAS:528:DC%2BD3cXltl2msLk%3D&md5=adf677eab643eb57059fdadcf2b4c56eCAS | 10871467PubMed |

Gibb, W. (1998). The role of prostaglandins in human parturition. Ann. Med. 30, 235–241.
The role of prostaglandins in human parturition.Crossref | GoogleScholarGoogle Scholar | 1:CAS:528:DyaK1cXlt1aht7g%3D&md5=cdc96c2743d5e3532313a9d16193cd77CAS | 9677008PubMed |

Gibbs, R. S., and Blanco, J. D. (1982). Premature rupture of the membranes. Obstet. Gynecol. 60, 671–679.
| 1:STN:280:DyaL3s%2FmtlOrsw%3D%3D&md5=572b51546fe5b2c34056d6dce1c8acbdCAS | 6755326PubMed |

Goldenberg, R. L., Hauth, J. C., and Andrews, W. W. (2000). Intrauterine infection and preterm delivery. N. Engl. J. Med. 342, 1500–1507.
Intrauterine infection and preterm delivery.Crossref | GoogleScholarGoogle Scholar | 1:STN:280:DC%2BD3c3ls1Oisg%3D%3D&md5=6720a76af9f7d13dea4eca182e6b8867CAS | 10816189PubMed |

Gomez, R., Ghezzi, F., Romero, R., Munoz, H., Tolosa, J. E., and Rojas, I. (1995). Premature labour and intra-amniotic infection. Clinical aspects and role of the cytokines in diagnosis and pathophysiology. Clin. Perinatol. 22, 281–342.
| 1:STN:280:DyaK2MvgtFGiuw%3D%3D&md5=5a9fac5d7230bc8e745465eaa7ae0685CAS | 7671540PubMed |

Keelan, J. A., Blumenstein, M., Helliwell, R. J. A., Sato, T. A., Marvin, K. W., and Mitchell, M. D. (2003). Cytokines, prostaglandins and parturition – a review. Placenta 24, S33–S46.
Cytokines, prostaglandins and parturition – a review.Crossref | GoogleScholarGoogle Scholar | 12842412PubMed |

Kim, I.-M., Ramakrishna, S., Gusarova, G. A., Yoder, H. M., Costa, R. H., and Kalinichenko, V. V. (2005). The forkhead box M1 transcription factor is essential for embryonic development of pulmonary vasculature. J. Biol. Chem. 280, 22 278–22 286.
The forkhead box M1 transcription factor is essential for embryonic development of pulmonary vasculature.Crossref | GoogleScholarGoogle Scholar | 1:CAS:528:DC%2BD2MXksl2ht74%3D&md5=0abf79687252ed2f752524dbb4e3dd66CAS |

Koo, C. Y., Muir, K. W., and Lam, E. W. (2012). FOXM1: From cancer initiation to progression and treatment. Biochim. Biophys. Acta 1819, 28–37.
FOXM1: From cancer initiation to progression and treatment.Crossref | GoogleScholarGoogle Scholar | 1:CAS:528:DC%2BC38XhsVeltw%3D%3D&md5=d2d409e66ebe4fa7b82e10b6304e8dc9CAS | 21978825PubMed |

Krupczak-Hollis, K., Wang, X., Kalinichenko, V. V., Gusarova, G. A., Wang, I. C., Dennewitz, M. B., Yoder, H. M., Kiyokawa, H., Kaestner, K. H., and Costa, R. H. (2004). The mouse Forkhead Box m1 transcription factor is essential for hepatoblast mitosis and development of intrahepatic bile ducts and vessels during liver morphogenesis. Dev. Biol. 276, 74–88.
The mouse Forkhead Box m1 transcription factor is essential for hepatoblast mitosis and development of intrahepatic bile ducts and vessels during liver morphogenesis.Crossref | GoogleScholarGoogle Scholar | 1:CAS:528:DC%2BD2cXpsVOluro%3D&md5=6d976ab59e04369caa35537af88513a0CAS | 15531365PubMed |

Lanoix, D., St-Pierre, J., Lacasse, A. A., Viau, M., Lafond, J., and Vaillancourt, C. (2012). Stability of reference proteins in human placenta: general protein stains are the benchmark. Placenta 33, 151–156.
Stability of reference proteins in human placenta: general protein stains are the benchmark.Crossref | GoogleScholarGoogle Scholar | 1:CAS:528:DC%2BC38Xit1eisLw%3D&md5=50d2552d5163f7869ebd9e81b5a1b650CAS | 22244735PubMed |

Lappas, M. (2013). NOD1 and NOD2 regulate proinflammatory and pro-labour mediators in human fetal membranes and myometrium via nuclear factor-kappa B. Biol. Reprod. 89, 14.
NOD1 and NOD2 regulate proinflammatory and pro-labour mediators in human fetal membranes and myometrium via nuclear factor-kappa B.Crossref | GoogleScholarGoogle Scholar | 23740944PubMed |

Lappas, M., and Permezel, M. (2011). The anti-inflammatory and antioxidative effects of nicotinamide, a vitamin B-3 derivative, are elicited by FoxO3 in human gestational tissues: implications for preterm birth. J. Nutr. Biochem. 22, 1195–1201.
The anti-inflammatory and antioxidative effects of nicotinamide, a vitamin B-3 derivative, are elicited by FoxO3 in human gestational tissues: implications for preterm birth.Crossref | GoogleScholarGoogle Scholar | 1:CAS:528:DC%2BC3MXhsFSktrzN&md5=fb49525b578693512f5fdc70cc4dafd5CAS | 21414766PubMed |

Lappas, M., Permezel, M., Georgiou, H. M., and Rice, G. E. (2002). Nuclear factor kappa B regulation of proinflammatory cytokines in human gestational tissues in vitro. Biol. Reprod. 67, 668–673.
Nuclear factor kappa B regulation of proinflammatory cytokines in human gestational tissues in vitro.Crossref | GoogleScholarGoogle Scholar | 1:CAS:528:DC%2BD38XlsFKqurw%3D&md5=45f3396c4e60eb24e86652d18fa4b034CAS | 12135912PubMed |

Lappas, M., Permezel, M., and Rice, G. E. (2003). N-acetyl-cysteine inhibits phospholipid metabolism, proinflammatory cytokine release, protease activity and nuclear factor-kappa B deoxyribonucleic acid-binding activity in human fetal membranes in vitro. J. Clin. Endocrinol. Metab. 88, 1723–1729.
N-acetyl-cysteine inhibits phospholipid metabolism, proinflammatory cytokine release, protease activity and nuclear factor-kappa B deoxyribonucleic acid-binding activity in human fetal membranes in vitro.Crossref | GoogleScholarGoogle Scholar | 1:CAS:528:DC%2BD3sXjtFCltr0%3D&md5=f1e1716847035bdfe80c7d88c214e605CAS | 12679464PubMed |

Lappas, M., Permezel, M., and Rice, G. E. (2006). 15-Deoxy-delta(12,14)-prostaglandin J(2) and troglitazone regulation of the release of phospholipid metabolites, inflammatory cytokines and proteases from human gestational tissues. Placenta 27, 1060–1072.
15-Deoxy-delta(12,14)-prostaglandin J(2) and troglitazone regulation of the release of phospholipid metabolites, inflammatory cytokines and proteases from human gestational tissues.Crossref | GoogleScholarGoogle Scholar | 1:CAS:528:DC%2BD28XpvFGhur8%3D&md5=68f164e6d2507e6f79694822d7b02a02CAS | 16434095PubMed |

Lappas, M., Lim, R., Riley, C., Rice, G. E., and Permezel, M. (2009a). Localisation and expression of FoxO1 proteins in human gestational tissues. Placenta 30, 256–262.
Localisation and expression of FoxO1 proteins in human gestational tissues.Crossref | GoogleScholarGoogle Scholar | 1:CAS:528:DC%2BD1MXhvF2kurc%3D&md5=8af15b31e8eea5c3bce9b16c2b0c0523CAS | 19150739PubMed |

Lappas, M., Riley, C., Rice, G. E., and Permezel, M. (2009b). Increased expression of ac-FoxO1 protein in prelabour fetal membranes overlying the cervix: possible role in human fetal membrane rupture. Reprod. Sci. 16, 635–641.
Increased expression of ac-FoxO1 protein in prelabour fetal membranes overlying the cervix: possible role in human fetal membrane rupture.Crossref | GoogleScholarGoogle Scholar | 1:CAS:528:DC%2BD1MXosVOrt70%3D&md5=a80d9a5a15cccb09ff063e5758379f53CAS | 19293131PubMed |

Lappas, M., Lim, R., Riley, C., Menon, R., and Permezel, M. (2010a). Expression and localisation of FoxO3 and FoxO4 in human placenta and fetal membranes. Placenta 31, 1043–1050.
Expression and localisation of FoxO3 and FoxO4 in human placenta and fetal membranes.Crossref | GoogleScholarGoogle Scholar | 1:CAS:528:DC%2BC3cXhsVyhsLvN&md5=2d1aa65b1163728491b520611cd00056CAS | 20934750PubMed |

Lappas, M., Riley, C., Barker, G., Rice, G., and Permezel, M. (2010b). Expression of FoxO4 in human placenta and fetal membranes: effect of human labour at term. Placenta 31, 1043–1050.
Expression of FoxO4 in human placenta and fetal membranes: effect of human labour at term.Crossref | GoogleScholarGoogle Scholar | 1:CAS:528:DC%2BC3cXhsVyhsLvN&md5=2d1aa65b1163728491b520611cd00056CAS | 20934750PubMed |

Lappas, M., Mitton, A., Lim, R., Barker, G., Riley, C., and Permezel, M. (2011). SIRT1 is a novel regulator of key pathways of human labour. Biol. Reprod. 84, 167–178.
SIRT1 is a novel regulator of key pathways of human labour.Crossref | GoogleScholarGoogle Scholar | 1:CAS:528:DC%2BC3MXlvVegu78%3D&md5=56156ec7337db5473373138e2cd380c1CAS | 20844277PubMed |

Lawn, J. E., Osrin, D., Adler, A., and Cousens, S. (2008). Four million neonatal deaths: counting and attribution of cause of death. Paediatr. Perinat. Epidemiol. 22, 410–416.
Four million neonatal deaths: counting and attribution of cause of death.Crossref | GoogleScholarGoogle Scholar | 18782248PubMed |

Lim, R., Riley, C., Barker, G., Rice, G. E., and Lappas, M. (2012). Human labour is associated with decreased cytoplasmic FoxO4. Placenta 33, 52–59.
Human labour is associated with decreased cytoplasmic FoxO4.Crossref | GoogleScholarGoogle Scholar | 1:CAS:528:DC%2BC38XhtlSqsg%3D%3D&md5=0646a6fbd52ed5582a94def52beac07dCAS | 22112832PubMed |

Lim, R., Barker, G., and Lappas, M. (2013a). SIRT6 is decreased with preterm labour and regulates key terminal effector pathways of human labour in fetal membranes. Biol. Reprod. 88, 17.
SIRT6 is decreased with preterm labour and regulates key terminal effector pathways of human labour in fetal membranes.Crossref | GoogleScholarGoogle Scholar | 23136298PubMed |

Lim, R., Barker, G., Riley, C., and Lappas, M. (2013b). Apelin is decreased with human preterm and term labour and regulates prolabour mediators in human primary amnion cells. Reprod. Sci. 20, 957–967.
Apelin is decreased with human preterm and term labour and regulates prolabour mediators in human primary amnion cells.Crossref | GoogleScholarGoogle Scholar | 23314958PubMed |

McLaren, J., Taylor, D. J., and Bell, S. C. (1999). Increased incidence of apoptosis in non-labour-affected cytotrophoblast cells in term fetal membranes overlying the cervix. Hum. Reprod. 14, 2895–2900.
Increased incidence of apoptosis in non-labour-affected cytotrophoblast cells in term fetal membranes overlying the cervix.Crossref | GoogleScholarGoogle Scholar | 1:STN:280:DC%2BD3c%2FhvVagtA%3D%3D&md5=d7b5c9cc0be3b228e12dc655bf8e8d2cCAS | 10548644PubMed |

Menon, R., Taylor, R. N., and Fortunato, S. J. (2010). Chorioamnionitis – a complex pathophysiologic syndrome. Placenta 31, 113–120.
Chorioamnionitis – a complex pathophysiologic syndrome.Crossref | GoogleScholarGoogle Scholar | 1:CAS:528:DC%2BC3cXhtlGjsL4%3D&md5=4761644cd0e00ffa7825e71e3e5048aeCAS | 20031205PubMed |

Mercer, B. M., and Lewis, R. (1997). Preterm labour and preterm premature rupture of the membranes. Diagnosis and management. Infect. Dis. Clin. North Am. 11, 177–201.
Preterm labour and preterm premature rupture of the membranes. Diagnosis and management.Crossref | GoogleScholarGoogle Scholar | 1:STN:280:DyaK2s3itVKhuw%3D%3D&md5=0c2c9b6a31d787ab91ca51bbc71ad4c1CAS | 9067791PubMed |

Mirza, M. K., Sun, Y., Zhao, Y. D., Potula, H. H., Frey, R. S., Vogel, S. M., Malik, A. B., and Zhao, Y. Y. (2010). FoxM1 regulates re-annealing of endothelial adherens junctions through transcriptional control of beta-catenin expression. J. Exp. Med. 207, 1675–1685.
FoxM1 regulates re-annealing of endothelial adherens junctions through transcriptional control of beta-catenin expression.Crossref | GoogleScholarGoogle Scholar | 1:CAS:528:DC%2BC3cXhtVejt7bJ&md5=9f99a4d7c55ae87a841f183e3ba5f6e9CAS | 20660612PubMed |

Mitchell, M. D., and Trautman, M. S. (1993). Molecular mechanisms regulating prostaglandin action. Mol. Cell. Endocrinol. 93, C7–C10.
Molecular mechanisms regulating prostaglandin action.Crossref | GoogleScholarGoogle Scholar | 1:CAS:528:DyaK3sXkvVKhu7c%3D&md5=e789e3f0cb0ffd0cd0240fb806060fd3CAS | 8349020PubMed |

Moore, R. M., Novak, J. B., Kumar, D., Mansour, J. M., Mercer, B. M., and Moore, J. J. (2009). Alpha-lipoic acid inhibits tumour necrosis factor-induced remodelling and weakening of human fetal membranes. Biol. Reprod. 80, 781–787.
Alpha-lipoic acid inhibits tumour necrosis factor-induced remodelling and weakening of human fetal membranes.Crossref | GoogleScholarGoogle Scholar | 1:CAS:528:DC%2BD1MXjvVSkur8%3D&md5=b5c476dfa22f78bff423fd15d583431eCAS | 19109223PubMed |

Myatt, S. S., and Lam, E. W. (2007). The emerging roles of forkhead box (Fox) proteins in cancer. Nat. Rev. Cancer 7, 847–859.
The emerging roles of forkhead box (Fox) proteins in cancer.Crossref | GoogleScholarGoogle Scholar | 1:CAS:528:DC%2BD2sXht1Wgsb%2FE&md5=a3febc697d94091f7065a1bc30ef169aCAS | 17943136PubMed |

Ning, Y., Li, Q. X., Xiang, H. L., Liu, F., and Cao, J. G. (2012). Apoptosis induced by 7-difluoromethoxyl-5,4 ‘-di-n-octyl genistein via the inactivation of FoxM1 in ovarian cancer cells. Oncol. Rep. 27, 1857–1864.
| 1:CAS:528:DC%2BC38XnvFektrk%3D&md5=584a7d9d54906b68da28ea7ff4b92f8dCAS | 22447287PubMed |

Parry, S., and Strauss, J. F. (1998). Premature rupture of the fetal membranes. N. Engl. J. Med. 338, 663–670.
Premature rupture of the fetal membranes.Crossref | GoogleScholarGoogle Scholar | 1:STN:280:DyaK1c7jsFGhsA%3D%3D&md5=a613c170a4042192ddf4634a504a77a6CAS | 9486996PubMed |

Petrou, S. (2005). The economic consequences of preterm birth during the first 10 years of life. BJOG 112, 10–15.
The economic consequences of preterm birth during the first 10 years of life.Crossref | GoogleScholarGoogle Scholar | 15715587PubMed |

Polzin, W. J., and Brady, K. (1998). The etiology of premature rupture of the membranes. Clin. Obstet. Gynecol. 41, 810–816.
The etiology of premature rupture of the membranes.Crossref | GoogleScholarGoogle Scholar | 1:STN:280:DyaK1M7hs1Clsg%3D%3D&md5=604422597549d048c1fcfee002e47477CAS | 9917935PubMed |

Roze, E., Kerstjens, J. M., Maathuis, C. G., ter Horst, H. J., and Bos, A. F. (2008). Risk factors for adverse outcome in preterm infants with periventricular haemorrhagic infarction. Pediatrics 122, e46–e52.
Risk factors for adverse outcome in preterm infants with periventricular haemorrhagic infarction.Crossref | GoogleScholarGoogle Scholar | 18541618PubMed |

Runić, R., Lockwood, C. J., LaChapelle, L., Dipasquale, B., Demopoulos, R. I., Kumar, A., and Guller, S. (1998). Apoptosis and Fas expression in human fetal membranes. J. Clin. Endocrinol. Metab. 83, 660–666.
Apoptosis and Fas expression in human fetal membranes.Crossref | GoogleScholarGoogle Scholar | 9467589PubMed |

Saigal, S., and Doyle, L. W. (2008). An overview of mortality and sequelae of preterm birth from infancy to adulthood. Lancet 371, 261–269.
An overview of mortality and sequelae of preterm birth from infancy to adulthood.Crossref | GoogleScholarGoogle Scholar | 18207020PubMed |

Sakata, M., Sado, T., Kitanaka, T., Naruse, K., Noguchi, T., Yoshida, S., Shigetomi, H., Onogi, A., Oi, H., and Kobayashi, H. (2008). Iron-dependent oxidative stress as a pathogenesis for preterm birth. Obstet. Gynecol. Surv. 63, 651–660.
Iron-dependent oxidative stress as a pathogenesis for preterm birth.Crossref | GoogleScholarGoogle Scholar | 18799020PubMed |

Shubert, P. J., Diss, E., and Iams, J. D. (1992). Etiology of preterm premature rupture of membranes. Obstet. Gynecol. Clin. North Am. 19, 251–263.
| 1:STN:280:DyaK38zjsVOlsQ%3D%3D&md5=a99d64dddd63492d637403de7a3e49caCAS | 1630736PubMed |

Uddin, S., Hussain, A. R., Ahmed, M., Siddiqui, K., Al-Dayel, F., Bavi, P., and Al-Kuraya, K. S. (2012). Overexpression of FoxM1 offers a promising therapeutic target in diffuse large B-cell lymphoma. Haematologica 97, 1092–1100.
Overexpression of FoxM1 offers a promising therapeutic target in diffuse large B-cell lymphoma.Crossref | GoogleScholarGoogle Scholar | 1:CAS:528:DC%2BC3sXjs1Whtg%3D%3D&md5=e73309bbf74544a58292fc46a3478a38CAS | 22271891PubMed |

Vadillo-Ortega, F., Hernandez, A., Gonzalez-Avila, G., Bermejo, L., Iwata, K., and Strauss, J. F. (1996). Increased matrix metalloproteinase activity and reduced tissue inhibitor of metalloproteinases-1 levels in amniotic fluids from pregnancies complicated by premature rupture of membranes. Am. J. Obstet. Gynecol. 174, 1371–1376.
Increased matrix metalloproteinase activity and reduced tissue inhibitor of metalloproteinases-1 levels in amniotic fluids from pregnancies complicated by premature rupture of membranes.Crossref | GoogleScholarGoogle Scholar | 1:CAS:528:DyaK28XjtFGrtLc%3D&md5=0f1b298eddaf5e0e2478486d2a4809adCAS | 8623872PubMed |

Wang, X., Bhattacharyya, D., Dennewitz, M. B., Kalinichenko, V. V., Zhou, Y., Lepe, R., and Costa, R. H. (2003). Rapid hepatocyte nuclear translocation of the forkhead box M1B (FoxM1B) transcription factor caused a transient increase in size of regenerating transgenic hepatocytes. Gene Expr. 11, 149–162.
Rapid hepatocyte nuclear translocation of the forkhead box M1B (FoxM1B) transcription factor caused a transient increase in size of regenerating transgenic hepatocytes.Crossref | GoogleScholarGoogle Scholar | 1:CAS:528:DC%2BD2cXis1ehsQ%3D%3D&md5=57f602d443c4ca9d50e05f94c84ff99eCAS | 14686788PubMed |

Wang, I. C., Meliton, L., Tretiakova, M., Costa, R. H., Kalinichenko, V. V., and Kalin, T. V. (2008). Transgenic expression of the forkhead box M1 transcription factor induces formation of lung tumours. Oncogene 27, 4137–4149.
Transgenic expression of the forkhead box M1 transcription factor induces formation of lung tumours.Crossref | GoogleScholarGoogle Scholar | 1:CAS:528:DC%2BD1cXot1ymu7g%3D&md5=f54b27532f0724e9bfbe6747a9418e6bCAS | 18345025PubMed |

Wierstra, I., and Alves, J. (2007). FOXM1, a typical proliferation-associated transcription factor. Biol. Chem. 388, 1257–1274.
FOXM1, a typical proliferation-associated transcription factor.Crossref | GoogleScholarGoogle Scholar | 1:CAS:528:DC%2BD2sXhsValtr%2FJ&md5=5f06c71e110afec541b4f3dad5548fa5CAS | 18020943PubMed |

Zhao, Y. Y., Gao, X. P., Zhao, Y. D., Mirza, M. K., Frey, R. S., Kalinichenko, V. V., Wang, I. C., Costa, R. H., and Malik, A. B. (2006). Endothelial cell-restricted disruption of FoxM1 impairs endothelial repair following LPS-induced vascular injury. J. Clin. Invest. 116, 2333–2343.
Endothelial cell-restricted disruption of FoxM1 impairs endothelial repair following LPS-induced vascular injury.Crossref | GoogleScholarGoogle Scholar | 1:CAS:528:DC%2BD28Xps1Sgs7c%3D&md5=b86f0204ea0f84e7628475946d9ee4f8CAS | 16955137PubMed |