Enhancement of ectopic β-human chorionic gonadotrophin expression by interferon-α

Iles, Ray K.; Chard, Tim

doi:10.1677/joe.0.1230501

Cited by 24 publications

(5 citation statements)

References 23 publications

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“…Iles and Chard [20] showed that interferon-alpha (IFN-alpha) enhances the ectopic production of the beta-subunit of hCG by bladder tumour cells. Iles and Chard also stated that their study suggested a direct transcription/translational effect of this cytokine (IFN-alpha) on the expression of a reproductive endocrine gene.…”

Section: Discussionmentioning

confidence: 99%

The expression of Beta Human Chorionic Gonadotrophin (beta-HCG) in human urothelial carcinoma)

Venyo¹,

Herring²,

Greenwood³

et al. 2011

Pan Afr Med Jrnl

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Introduction Studies regarding the immuno-histological expression and relevance of Beta-Human Chorionic Gonadotrophin (=-HCG) in urothelial carcinoma are few. There is also no clear cut way of predicting exactly which superficial urothelial carcinomas would subsequently recur or progress and which muscle-invasive urothelial tumours would progress. The objective of the study was to study the immunohistological expression of =-HCG in urothelial carcinoma with regards to grade, category and outcome following treatment Methods The expression of =-HCG in urothelial carcinomas of 86 patients was studied with regards to grade, stage and outcome using an immunohistological (ABC) method and formalin fixed/paraffin embedded tumours. Results Of the 86 tumours (55 superficial and 31 muscle-invasive) studied 45, 16 and 26 were graded as G1, G2, and G3 respectively. Thirteen of the 55 superficial tumours were positively stained for β=-HCG and 42 negatively stained. Twenty of the 31 muscle-invasive tumours studied were positively stained for β=-HCG and 11 were negative. Of the 13 β=-HCG positive superficial tumours only one did not recur at follow up and 12 subsequently recurred, of the 42 β=-HCG negative superficial tumours 19 did not recur and 23 recurred. Only one of twenty patients with β=-HCG positive muscle-invasive tumours survived; 6 of 11 patients with β=-HCG negative muscle-invasive tumours survived. The results indicate that positive staining of the tumours was more commonly associated with tumours of higher grade, higher stage and inferior outcome. Conclusion The Immunohistological expression of β=-HCG would likely predict superficial tumours that would recur and muscle-invasive tumours with inferior outcome.

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Section: Discussionmentioning

confidence: 99%

The expression of Beta Human Chorionic Gonadotrophin (beta-HCG) in human urothelial carcinoma)

Venyo¹,

Herring²,

Greenwood³

et al. 2011

Pan Afr Med Jrnl

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“…72 IFNA protein present in syncytiotrophoblast 93 is released from explant cultures of human trophoblast 88 and, of particular importance, IFNA may stimulate transcription of the CGB gene without effects on cell proliferation. 94 However, this effect of IFNA on CGB production by bladder tumor cell lines has not been confirmed using trophectoderm cells.…”

Section: Interferons and Uterine Receptivity In Primatesmentioning

confidence: 96%

Interferons and Uterine Receptivity

2009

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This article focuses on the potential roles of interferons (IFNs) in establishing uterine receptivity to implantation. A common feature of the peri-implantation period of pregnancy in most mammals is production of type I and/or type II IFNs by trophoblasts that induce and/or stimulate expression of an array of IFN-stimulate genes (ISGs). These effects range from pregnancy recognition signaling in ruminants through IFN tau to effects on cellular functions of the uterus and uterine vasculature. For actions of IFNs, progesterone (P4) is permissive to the expression of many effects and to the expression of ISGs that are induced directly by an IFN or induced by P4 and stimulated by an IFN in a temporal and/or cell-specific manner. Uterine receptivity to implantation is P4 dependent; however, implantation events are preceded by loss of expression of progesterone (PGR) and estrogen (ESR1) receptors by uterine epithelia. Therefore, P4 likely acts via PGR-positive stromal cells to induce expression of fibroblast growth factors-7 and -10 and/or hepatocyte growth factor (progestamedins) that then act via their respective receptors on uterine epithelia and trophectoderm to affect expression of ISGs. The permissive effects of P4 on the expression of ISGs and the effects of P4 to induce and IFNs to stimulate gene expression raise the question of whether uterine receptivity to implantation requires P4 and IFN to activate unique, but complementary, cell signaling pathways. Uterine receptivity to implantation, depending on species, involves changes in the expression of genes for the attachment of trophectoderm to the uterine lumenal epithelium (LE) and superficial glandular epithelium (sGE), modification of the phenotype of uterine stromal cells, the silencing of PGR and ESR1 genes, the suppression of genes for immune recognition, alterations in membrane permeability to enhance conceptus-maternal exchange of factors, increased vascularity of the endometrium, activation of genes for transport of nutrients into the uterine lumen, and enhanced signaling for pregnancy recognition. Differential expression of genes by uterine LE/sGE, mid- to deep-glandular epithelia (GE), and stromal cells in response to P4 and IFNs is likely to influence uterine receptivity to implantation in most mammals. Understanding the roles of IFNs in uterine receptivity for implantation is necessary to develop approaches to enhance reproductive health and fertility in humans and domestic animals.

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“…The shift in endometrial production from PGF to PGE is associated with implantation and, in humans, IFNA suppresses P 4 -regulated production of basal PGF, but not PGE 2 (Mitchell & Smith 1992). Of particular interest is the report that IFNA may stimulate transcription of the CGB gene without effects on cell proliferation (Iles & Chard 1989); however, these results are from studies using a bladder tumor cell line, which have not been confirmed using trophectoderm cells.…”

Section: Ifns and Uterine Receptivity In Primatesmentioning

confidence: 99%

Comparative aspects of implantation

Bazer

Spencer²,

Johnson³

et al. 2009

Reproduction

345

285

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Uterine receptivity to implantation of blastocysts in mammals includes hatching from zona pellucida, precontact with uterine luminal (LE) and superficial glandular (sGE) epithelia and orientation of blastocyst, apposition between trophectoderm and uterine LE and sGE, adhesion of trophectoderm to uterine LE/sGE, and, in some species, limited or extensive invasion into the endometrial stroma and induction of decidualization of stromal cells. These peri-implantation events are prerequisites for pregnancy recognition signaling, implantation, and placentation required for fetal-placental growth and development through the remainder of pregnancy. Although there is a range of strategies for implantation in mammals, a common feature is the requirement for progesterone (P 4 ) to downregulate expression of its receptors in uterine epithelia and P 4 prior to implantation events. P 4 then mediates its effects via growth factors expressed by stromal cells in most species; however, uterine luminal epithelium may express a growth factor in response to P 4 and/or estrogens in species with a true epitheliochorial placenta. There is also compelling evidence that uterine receptivity to implantation involves temporal and cell-specific expression of interferon (IFN)-stimulated genes that may be induced directly by an IFN or induced by P 4 and stimulated by an IFN. These genes have many roles including nutrient transport, cellular remodeling, angiogenesis and relaxation of vascular tissues, cell proliferation and migration, establishment of an antiviral state, and protection of conceptus tissues from challenges by the maternal immune cells.

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Enhancement of ectopic β-human chorionic gonadotrophin expression by interferon-α

Cited by 24 publications

References 23 publications

The expression of Beta Human Chorionic Gonadotrophin (beta-HCG) in human urothelial carcinoma)

The expression of Beta Human Chorionic Gonadotrophin (beta-HCG) in human urothelial carcinoma)

Interferons and Uterine Receptivity

Comparative aspects of implantation

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