Seladin-1 as a target of estrogen receptor activation in the brain: A new gene for a rather old story?

Peri, Alessandro; Danza, Giovanna; Serio, Mario

doi:10.1007/bf03345387

Cited by 10 publications

(7 citation statements)

References 50 publications

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“…Dhcr24 also mediates anti-apoptotic and anti-oxidative activities by inhibiting the activation of caspase 3, one of the key modulators of apoptosis, and binding to p53 to displace Mdm2, resulting in p53, a tumor suppressor, accumulation [85]. Dhcr24 gene is activated by ER in neurons and glia cells [86] and by AR in prostate cells [87] and rat glioma C6 cells [88]. The androgen-responsiveness of Dhcr24 may be mediated by the direct action of AR because an androgen responsive element (ARE) is present in the human DHCR24 promoter (-4384 to -2892 bp) [87].…”

Section: Discussionmentioning

confidence: 99%

Effects of Prenatal Testosterone Exposure on Sexually Dimorphic Gene Expression in the Neonatal Mouse Cortex and Hippocampus

Armoskus

Mota

Moreira

et al. 2013

J Steroids Horm Sci

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Objective Using gene expression microarrays and reverse transcription with quantitative polymerase chain reaction (RT-qPCR), we have recently identified several novel genes that are differentially expressed in the neonatal male versus female mouse cortex/hippocampus (Armoskus et al.). Since perinatal testosterone (T) secreted by the developing testes masculinizes cortical and hippocampal structures and the behaviors regulated by these brain regions, we hypothesized that sexually dimorphic expression of specific selected genes in these areas might be regulated by T during early development. Methods To test our hypothesis, we treated timed pregnant female mice daily with vehicle or testosterone propionate (TP) starting on embryonic day 16 until the day of birth. The cortex/hippocampus was collected from vehicle- and TP-treated, male and female neonatal pups. Total RNA was extracted from these brain tissues, followed by RT-qPCR to measure relative mRNA levels of seven sex chromosome genes and three autosomal genes that have previously showed sex differences. Results The effect of prenatal TP was confirmed as it stimulated Dhcr24 expression in the neonatal mouse cortex/hippocampus and increased the anogenital distance in females. We found a significant effect of sex, but not TP, on expression of three Y-linked (Ddx3y, Eif2s3y, and Kdm5d), four X-linked (Eif2s3x, Kdm6a, Mid1, and Xist), and one autosomal (Klk8) genes in the neonatal mouse cortex/hippocampus. Conclusion Although most of the selected genes are not directly regulated by prenatal T, their sexually dimorphic expression might play an important role in the control of sexually differentiated cognitive and social behaviors as well as in the etiology of sex-biased neurological disorders and mental illnesses.

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Section: Discussionmentioning

confidence: 99%

Effects of Prenatal Testosterone Exposure on Sexually Dimorphic Gene Expression in the Neonatal Mouse Cortex and Hippocampus

Armoskus

Mota

Moreira

et al. 2013

J Steroids Horm Sci

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“…Estrogen is important throughout development, not only for regulating female reproductive systems but also bone formation (59) and brain development (60). Increased ER activity FIGURE 6.…”

Section: Discussionmentioning

confidence: 99%

Identification of Flightless-I as a Substrate of the Cytokine-independent Survival Kinase CISK

Xu¹,

Liao

Qin

et al. 2009

Journal of Biological Chemistry

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Phosphatidylinositol (PI) 3-kinase mediates multiple pathways that regulate many aspects of the cell including metabolism, survival, migration, and proliferation. Both Akt and cytokine-independent survival kinase (CISK)/SGK3 are known AGC family protein kinases that function downstream of PI 3-kinase. Although the Akt signaling pathway has been studied extensively, the specific signaling cascades that are modulated by CISK remain to be elucidated. To understand CISK function, we affinity-purified the CISK protein complex and identified Flightless-I (FLII) as a novel downstream target of CISK. Here we show that FLII is an in vivo substrate of CISK that functions downstream of PI 3-kinase. CISK can associate with FLII and phosphorylate FLII at residues Ser 436 and Thr 818 . FLII has been shown to act as a co-activator for nuclear hormone receptors such as estrogen receptor (ER). We demonstrate here that CISK can enhance ER transcription, which is dependent on its kinase activity, and mutation of CISK phosphorylation sites on FLII attenuates its activity as an ER co-activator. Furthermore, FLII knockdown by RNA interference renders 32D cells more sensitive to interleukin-3 withdrawal-induced apoptosis, suggesting that FLII itself is also a survival factor. These findings support the model that CISK phosphorylates FLII and activates nuclear receptor transcription and suggest a new cell survival signaling pathway mediated by PI 3-kinase and CISK.

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“…The 7-dehydrocholestrol reductase (DHCR7) gene, which encodes an enzyme that catalyzes production of the hormone precursor cholesterol by reduction of the C7-C8 double bond of 7-dehydrocholesterol [64], and the gene for stearol-CoA desaturase (SCD), which can contribute to increased cholesterol synthesis [65], were increased 1.6-and 2.0-fold by 25 lM genistein, respectively. In contrast to the above, the 24-dehydrocholestrol reductase (DHCR24), also known as seladin-1, which contributes to cholesterol synthesis by catalyzing the reduction of the delta-24 double bond of sterol intermediates [66], was down-regulated by lowconcentration genistein only. Thus, the main effect on these steroid and other metabolizing enzymes appears to be an increase in gene transcription at high genistein concentrations that could contribute to increased cholesterol synthesis, increased hormone metabolism and decreased hormone signaling that potentially contribute to decreased growth in cells exposed to !…”

Section: Effects Of Genistein On Apoptosis-related Genesmentioning

confidence: 97%

Concentration-dependent effects of genistein on global gene expression in MCF-7 breast cancer cells: an oligo microarray study

Lavigne

Takahashi

Chandramouli

et al. 2007

Breast Cancer Res Treat

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Breast cancer is the most commonly diagnosed cancer among US women; there is therefore great interest in developing preventive and treatment strategies for this disease. Because breast cancer incidence is much lower in countries where women consume high levels of soy, bioactive compounds in this food source have been studied for their effects on breast cancer. Genistein, found at high levels in soybeans and soy foods, is a controversial candidate breast cancer preventive phytochemical whose effects on breast cells are complex. To understand more clearly the molecular mechanisms underlying the effects of genistein on breast cancer cells, we used a DNA oligo microarray approach to examine the global gene expression patterns in MCF-7 breast cancer cells at both physiologic (1 or 5 microM) and pharmacologic (25 microM) genistein concentrations. Microarray analyses were performed on MCF-7 cells after 48 h of either vehicle or 1, 5, or 25 microM genistein treatment. We found that genistein altered the expression of genes belonging to a wide range of pathways, including estrogen- and p53-mediated pathways. At 1 and 5 microM, genistein elicited an expression pattern suggestive of increased mitogenic activity, confirming the proliferative response to genistein observed in cultured MCF-7 cells, while at 25 microM genistein effected a pattern that likely contributes to increased apoptosis, decreased proliferation and decreased total cell number, also consistent with cell culture results. These findings provide evidence for a molecular signature of genistein's effects in MCF-7 cells and lay the foundation for elucidating the mechanisms of genistein's biological impact in breast cancer cells.

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Seladin-1 as a target of estrogen receptor activation in the brain: A new gene for a rather old story?

Cited by 10 publications

References 50 publications

Effects of Prenatal Testosterone Exposure on Sexually Dimorphic Gene Expression in the Neonatal Mouse Cortex and Hippocampus

Effects of Prenatal Testosterone Exposure on Sexually Dimorphic Gene Expression in the Neonatal Mouse Cortex and Hippocampus

Identification of Flightless-I as a Substrate of the Cytokine-independent Survival Kinase CISK

Concentration-dependent effects of genistein on global gene expression in MCF-7 breast cancer cells: an oligo microarray study

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