Steroid-Modulated Proliferation of Human Endometrial Carcinoma Cell Lines: Any Role for Insulin-like Growth Factor Signaling?

Gielen, Susanne C.J.P.; Hanekamp, Eline E.; Blok, Leen J.; Huikeshoven, Frans J.M.; Burger, Curt W.

doi:10.1016/j.jsgi.2004.08.003

Cited by 21 publications

(17 citation statements)

References 34 publications

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“…We observed altered transcript levels of genes encoding for the insulin-like growth factor (IGF) signaling system, which can be influenced by ER and have been implicated in the lung oncogenic process (Gielen et al, 2005). The aberrant expression of insulin-like growth factors, such as IGFR2, is observed in the fetal mouse lung exposed to arsenic in utero (Shen et al, 2007) and in arsenic-exposed neonatal liver.…”

Section: Discussionmentioning

confidence: 97%

Aberrant DNA methylation and gene expression in livers of newborn mice transplacentally exposed to a hepatocarcinogenic dose of inorganic arsenic

et al. 2007

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Our prior work showed that brief exposure of pregnant C3H mice to inorganic arsenic-induced hepatocellular carcinoma (HCC) formation in adult male offspring. The current study examined the early hepatic events associated with this oncogenic transformation. Pregnant mice were exposed to a known carcinogenic dose of arsenic (85 ppm) in the drinking water from gestation days 8 to 18. The dams were allowed to give birth and liver samples from newborn males were analyzed for arsenic content, global DNA methylation and aberrant expression of genes relevant to the carcinogenic process. Arsenic content in newborn liver reached 57 ng/g wet weight, indicating arsenic had crossed the placenta, reached the fetal liver and that significant amounts remained after birth. Global methylation status of hepatic DNA was not altered by arsenic in the newborn. However, a significant reduction in methylation occurred globally in GC-rich regions. Microarray and real-time RT-PCR analysis showed that arsenic exposure enhanced expression of genes encoding for glutathione production and caused aberrant expression of genes related to insulin growth factor signaling pathways and cytochrome P450 enzymes. Other expression alterations observed in the arsenictreated male mouse newborn liver included the overexpression of cdk-inhibitors and stress response genes including increased expression of metallothionein-1 and decreased expression of betainehomocysteine methyltransferase and thioether S-methyltransferase. Thus, transplacental exposure to arsenic at a hepatocarcinogenic dose induces alterations in DNA methylation and a complex set of aberrant gene expressions in the newborn liver, a target of arsenic carcinogenesis.

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Section: Discussionmentioning

confidence: 97%

Aberrant DNA methylation and gene expression in livers of newborn mice transplacentally exposed to a hepatocarcinogenic dose of inorganic arsenic

et al. 2007

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“…Proliferation of the ECC-1 cells was quantified as described by Gielen et al [14] with some minor modifications. Cells were cultured in assay medium (DMEM/F12 medium, without phenol red supplemented with 5% csFBS) for 5 days before starting the experiment.…”

Section: Cell Proliferation Assaysmentioning

confidence: 99%

“…The T47D cell line is not often used for proliferative assays, but it is the host cell in many developed transcriptional activation assays [11][12][13]. The ECC-1 cell line is an endometrium cell line that also proliferates under the influence of estrogens and was included because it is derived from a target tissue, which is actually examined in the in vivo uterotrophic assay [14]. In addition, the BG-1 cell line was included because it represents the ovary, another main female estrogen-sensitive tissue [15].…”

Section: Introductionmentioning

confidence: 99%

Proliferation assays for estrogenicity testing with high predictive value for the in vivo uterotrophic effect

Wang

Aarts

Evers

et al. 2012

The Journal of Steroid Biochemistry and Molecular Biology

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“…In a series of experiment where the IGF signalling pathway was investigated, Gielen et al [4] could show that IGF signalling indeed plays a role in estrogen-induced growth regulation of endometrial cells and that the IGFBPs were differentially regulated by estogens compared with progestagens (IGFBP3 and IGFBP6 were downregulated by progesterone and IGFBP4 is upregulated by estradiol).…”

Section: Estrogen Receptormentioning

confidence: 99%

Investigations into the molecular background of endometrial cancer

Blok

Burger

2005

International Congress Series

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Steroid-Modulated Proliferation of Human Endometrial Carcinoma Cell Lines: Any Role for Insulin-like Growth Factor Signaling?

Abstract: Estrogen-induced stimulation of proliferation of ECC-1 endometrial cancer cells is partly achieved via IGF signaling. Furthermore, the IGFBPs are regulated by estrogens as well as progestagens and could potentially play a role in the modulation of endometrial cancer cell proliferation.

Cited by 21 publications

References 34 publications

Aberrant DNA methylation and gene expression in livers of newborn mice transplacentally exposed to a hepatocarcinogenic dose of inorganic arsenic

Aberrant DNA methylation and gene expression in livers of newborn mice transplacentally exposed to a hepatocarcinogenic dose of inorganic arsenic

Proliferation assays for estrogenicity testing with high predictive value for the in vivo uterotrophic effect

Investigations into the molecular background of endometrial cancer

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