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Regulation of Cell Functions
Published in Enrique Pimentel, Handbook of Growth Factors, 2017
Analysis of cDNAs corresponding to cMG1 indicates that it encodes a protein of 338 amino acids and shows no similarities to other genes with the exception of TIS11, a gene induced by phorbol ester in 3T3 mouse fibroblasts. The two genes, cMG1 and TIS11, appear to code for early response gene products. A member of the set of immediate-early genes expressed in mouse 3T3 cells, cyr61, encodes a polypeptide of 379 amino acids which contains several cysteine residues.225-226 The Cyr-61 protein is expressed minutes after cell stimulation with serum, PDGF, or FGF. Cyr-61 has a short half-life and is a secreted protein that is associated with the extracellular matrix, suggesting that it may function in cell-to-cell communication. The Cyr-61 protein binds heparin and shows similarities with the product of the int-1 proto-oncogene. Another immediate-early gene, 3CH134, whose transcription is rapidly and transiently stimulated by serum growth factors, encodes a 367-amino acid protein of 40 kDa that does not share similarity with any known protein.227 The products of late growth-regulated genes have varied functions in addition to the participation of some of them in the DNA replication machinery. Two human genes required for G1 progression were identified by their ability to complement the mutations of ts cell cycle mutants isolated from the BHK-21 Syrian hamster cell line.228 These two genes were assigned to human chromosome regions 7cen-q35 and 8q21, respectively, and one of them corresponds to the gene encoding asparagine synthetase. The function of the other gene is unknown.
Molecular diagnosis of endometriosis
Published in Carlos Simón, Linda C. Giudice, The Endometrial Factor, 2017
Lusine Aghajanova, Linda C. Giudice
Evidence for P4 resistance in eutopic endometrium from women with endometriosis also comes from several global comparative microarray analyses of eutopic and ectopic endometrial tissue from women with versus without disease (reviewed in (74)). Our group performed the first such analysis comparing the endometrial transcriptome from women with minimal or mild endometriosis with no disease during the midsecretory endometrium (MSE) phase, when P4 is at its peak (75). We found 91 and 115 genes significantly up- and downregulated >2-fold, respectively (75). Several P4-regulated genes (Table 4.1), normally upregulated during the window of implantation, were downregulated in MSE of women with endometriosis (75). In a subsequent study, we performed global analysis of the eutopic endometrial transcriptome throughout the menstrual cycle from women with and without moderate to severe endometriosis (34). Interestingly, comparative analysis of different cycle phases with and without endometriosis revealed that the largest number of statistically significantly differentially expressed genes between the two groups was in ESE (34). On principal component analysis (PCA), ESE samples from women with endometriosis clustered closer to PE samples rather than MSE samples. Several P4-regulated genes (Table 4.1) were downregulated in ESE and MSE in women with disease, while PR was upregulated in ESE, suggesting resistance to the actions of endogenous P4 (34). Remarkably, evaluation of LSE in women with endometriosis compared with disease-free subjects is not informative (76). Absenger et al. (77) also reported on differential gene expression in the eutopic endometrium from women with endometriosis compared with controls in the proliferative and secretory cycle phases that suggested Cyr61 (cysteine-rich angiogenic inducer 61, CCN1) as a cycle-independent biomarker for endometriosis. It was also upregulated in endometriotic lesions, and the results were confirmed in a nude mouse xenograft model of endometriosis (77). The proposed role for Cyr61 in the pathogenesis of endometriosis is likely associated with facilitating adhesions and angiogenesis (77). As a consequence, we believe that genomic profiling of endometrial tissue could potentially revolutionize the noninvasive diagnostics of endometriosis.
Pathophysiology behind adipose tissue deposition in lymphedema and how liposuction can completely reduce excess volume
Published in Byung-Boong Lee, Peter Gloviczki, Francine Blei, Jovan N. Markovic, Vascular Malformations, 2019
Other research regarding adipose tissue deposition includes the following: The findings of increased adipose tissue in intestinal segments in patients with Crohn disease, known as “fat wrapping,” have clearly shown that inflammation plays an important role.21, 25Tonometry can distinguish if a lymphedematous arm is harder or softer than a contralateral arm (if unaffected). If a lower tissue tonicity value is recorded in the edematous arm, it indicates that there is accumulated lymph fluid in the tissue, and these patients are candidates for conservative treatment methods. In contrast, patients with a harder arm, compared with the healthy one, have an adipose tissue excess that can successfully be removed by liposuction.8In Graves ophthalmopathy, a major problem is an increase in the intraorbital adipose tissue volume leading to exophthalmos. Adipocyte-related immediate early genes (IEGs) are overexpressed in active ophthalmopathy and cysteine-rich, angiogenic inducer 61 (CYR61) may have a role in both orbital inflammation and adipogenesis and serve as a marker of disease activity.26Preoperative investigation with volume-rendered computer tomography (VRCT) images showed a significant preoperative increase of adipose tissue in the swollen arm, the excess volume consisting of 81% (range 68%–96%) fat.11Analyses with dual x-ray absorptiometry (DXA) that was compared to plethysmography in 18 women with arm lymphedema following a mastectomy showed a significant increase of adipose tissue, 73% (range, 43%–111%), in the nonpitting swollen arm before surgery.12Adipogenesis in response to lymphatic fluid stasis is associated with a marked mononuclear cell inflammatory response.27Lymphatic fluid stasis potently upregulates the expression of fat differentiation markers both spatially and temporally.28The underlying pathophysiology of lymphedema drives adipose-derived stem cells toward adipogenic differentiation.29Consecutive analyses of the content of the aspirate removed under bloodless conditions using a tourniquet, showed a very high content of adipose tissue in 105 women with postmastectomy arm lymphedema (mean 94%, range 58%–100%).3
KRas-ERK signalling promotes the onset and maintenance of uveal melanoma through regulating JMJD6-mediated H2A.X phosphorylation at tyrosine 39
Published in Artificial Cells, Nanomedicine, and Biotechnology, 2019
Yaping Li, Peng Yu, Ying Zou, Wenrui Cai, Weixuan Sun, Ning Han
CYR61 is a connective tissue growth factor which has been considered as a crucial mediator in the developing and metastasis of cancers [26]. High expression of CYR61 was present in cervical cancer [27] and oesophageal squamous cell carcinoma [28], and exerted diverse functions in several types of cancers [29]. In malignant melanoma, CYR61 worked as a biomarker for tumour cells proliferation and metastasis, making it a potential target for melanoma treatment [30]. Apart from CYR61, IGFBP3 [31], WNT16B [32], NT5E [33], GDF15 [34] and CARD16 [35] have been demonstrated as tumour-relevant genes (tumour-promoter or tumour-suppressor) in some cancers. By performing qRT-PCR, CYR61, IGFBP3 and WNT16B were negatively regulated, while NT5E, GDF15 and CARD16 were positively regulated through H2A.XY39ph. Besides, ChIP assay results implied that ERK1/2 downstream genes’ transcription which was closely associated with tumour progression could be regulated by H2A.XY39ph. These findings further confirmed the involvement of H2A.XY39ph in uveal melanoma cells growth and migration.
Ras-AKT signaling represses the phosphorylation of histone H1.5 at threonine 10 via GSK3 to promote the progression of glioma
Published in Artificial Cells, Nanomedicine, and Biotechnology, 2019
Ben Sang, Jianjing Sun, Dongxu Yang, Zhen Xu, Yuzhen Wei
To further confirm the tumor-suppressive role of H1.5T10ph in cancer, the regulatory effects of H1.5T10ph on the transcription of Ras downstream genes were studied, including CYR61, IGFBP3, WNT16B, NT5E, GDF15, and CARD16. These factors are all pivotal regulators in the tumor as well. Among which, CYR61, IGFBP3, WNT16B, and NT5E were reported to be oncogenes while GDF15 and CARD16 were considered as tumor suppressors. In different solid tumors, CYR61 was shown to promote tumor growth and vascularization as well as cell invasiveness and metastasis [24,25]. Like CYR61, overexpression of WNT16B promoted tumor growth and chemotherapy resistance [26]. Depletion of IGFBP3 [27] or NT5E [28] induced tumor cell loss and thereby suppressed tumor cells growth. Of contrast, in vitro and in vivo experiments suggested overexpression of GDF15 [29] or CARD16 [30] inhibited tumor cell growth via controlling caspases and cell proliferation, respectively. The findings of this study demonstrated that H1.5T10ph was capable of regulating the transcription of these genes, further confirmed the involvement of H1.5T10ph in the progression of glioma.
Serum CYR61 Is Associated with Disease Activity in Graves’ Orbitopathy
Published in Ocular Immunology and Inflammation, 2018
Young Jun Woo, Yuri Seo, Jin Joo Kim, Ji Won Kim, Yil Park, Jin Sook Yoon
Cysteine-rich angiogenic inducer 61 (CYR61), also called CCN1, is a secreted extracellular matrix (ECM)-related signaling protein that is encoded by the immediate early gene.4,5 CYR61 has been demonstrated to regulate various cellular activities, including cell proliferation, migration, adhesion, and apoptosis.6 Moreover, several studies have established that CYR61 plays a particularly important role in inflammation.2 In most adult tissues, CYR61 is maintained at low levels under homeostatic conditions,7 but is increased in inflammatory conditions such as rheumatoid arthritis (RA),8 bacterial and viral infection,7 diabetic nephropathy and retinopathy,6 colon inflammation,9 and many types of cancers.5 In addition, serum CYR61 levels have been reported to be higher in inflammatory conditions, including systemic lupus erythematosus (SLE), and were associated with disease activity.1