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Insights into the role of estrogen-related receptors α, β and γ in tumor Leydig cells

Posted by M Kotula-Balak, A Milon, P Pawlicki, et al. on 2018-04-22 19:52:35


In this study, we demonstrate, for the first time, estrogen-related receptor (ERR) regulation of the physiological and biochemical status of testicular tumor Leydig cells.

In a mouse tumor Leydig cells, ERRs (alpha, beta, and gamma) were silenced via siRNA. Cell morphology and cell physiology (proliferation and observation of monolayer formation) were observed by inverted phase-contrast microscope. Leydig cell functional markers (steroid receptors and signaling molecules) were examined by immunofluorescence and Western blotting. Additionally, progesterone secretion was assessed. Mitochondrial mass and membrane potential were analyzed by flow-cytometry while cGMP and Ca2+ concentrations were analyzed using immunoenzymatic and colorimetric assays, respectively.

These results revealed, ERRs indirectly regulate Leydig cell proliferation while ERRalpha and beta affect cell monolayer formation. ERRs interact with canonical and membrane estrogen receptors (ERalpha, ERbeta, and GPER), androgen receptor, metalloproteinase (MMP 9), protein kinase A (PKA), extracellular-regulated kinase (ERK), and neurogenic locus notch homolog protein 2 (Notch2). Depending on the type of ERR knocked down, coupled with estradiol treatment, changes in progesterone concentration and cGMP and Ca2+ concentrations constitute a microenvironment that may effect tumor Leydig cell characteristics. ERRs should be considered important factors in developing of innovating approaches that target pathological processes of testicular Leydig cells.

Relation of locus 1p13 rs646776 polymorphism with the risk of preeclampsia

Posted by R H. Emam, M H. Ghattas, N M. Mesbah, et al. on 2018-03-26 19:07:44


Objective: This study aimed to assess the relation of locus 1p13 rs646776 (T/C) polymorphism with preeclampsia in Egyptian women.

Methods: The study included 100 healthy pregnant female subjects and 100 preeclampsia patients. The genotypes of the polymorphisms were assessed. Endothelin-1 level was determined in plasma.

Results: The major T allele of the 1p13.3 genomic region rs646776 polymorphism had a higher frequency in preeclampsia patients. Carriers of C allele had significantly lower endothelin-1 levels, lower systolic and diastolic blood pressure, decreased proteinuria, and increased HDL-C in the patients.

Conclusion: The rare C allele of rs646776 polymorphism in chromosomal locus 1p13.3 is associated with decreased risk of preeclampsia.


Esophageal squamous cell carcinoma (ESCC) is one of the most malignant tumors in China with a poor prognosis. Most ESCC patients were diagnosed at advanced stages, losing the opportunity for surgical excision. Hence, it remains a pressing work to identify biomarkers for early detection, prognosis prediction and targeting therapies in ESCC. Interferon-stimulated gene 15 (ISG15) encodes a 15-kDa protein, and is involved in the post-translational modification (PTMs) of multiple proteins. However, the molecular functions of ISG15 in ESCC remain unclear. In this work, we found that ISG15 was aberrantly expressed in ESCC tissues and cell lines. Enhanced protein level of ISG15 promoted cellular malignant phenotypes including proliferation, migration, invasion and tumor formation in vivo. Consistently, reduction of ISG15 attenuated the cellular malignant phenotype in ESCC cell lines. Furthermore, gene-expression profiles suggested that the differentially expressed ISG15 affected the expression of a panel of genes enriched in the cell adherens junction, such as c-MET. Notably, as a secreted protein, the concentration of ISG15 was elevated in ESCC plasma than healthy individuals, acting as a potential diagnostic marker. Taken together, our results suggested a tumor promotion role of ISG15 in ESCC via c-MET/Fyn/beta-catenin pathway.



The aim of the present study was to search for predictive and prognostic factors in patients with metastatic renal cell carcinoma (mRCC) treated with everolimus among the components of the WNT/beta-catenin pathway.

Patients and Methods

In a prospective, single-arm, phase II study, patients with mRCC received everolimus (10 mg/d) in a 30-day cycle. We performed a prospectively planned evaluation of the potential biomarkers of the WNT/beta-catenin pathway.


The serum level of soluble E-cadherin (sE-cadherin) in patients with RCC was significantly greater than that in the controls (71.62±22.28 pg/mL vs. 54.26±10.317 pg/mL; P =.0069). After 2 cycles of everolimus therapy, we observed a significance increase in sE-cadherin (from 71.81±21.18 pg/mL to 77.50±28.212 pg/mL; P =.0151). The Dickkopf-1 protein levels in the study and control groups were not significantly different (P=.2135). The favorable independent predictors for everolimus therapy were normal lactate dehydrogenase level before treatment (hazard ratio [HR], 0.52; 95% confidence interval [CI], 0.28-0.98; P =.0443) and low sE-cadherin level (HR, 0.54; 95% CI, 0.29-0.98; P =.0422). On multivariate analysis, we observed that worse overall survival was seen in patients with a lower regression coefficient of sE-cadherin after 2 cycles of treatment (HR, 2.60; 95% CI, 1.23-5.52; P =.0128), an increased corrected calcium level (HR, 3.09; 95% CI, 1.21-7.88; P = .0180), and an increased lactate dehydrogenase level before treatment (HR, 1.98; 95% CI, 1.02-3.83; P = .0426).


WNT/beta-catenin component expression in patients with mRCC had no effect on progression-free survival or overall survival. However, we found that the sE-cadherin level might interact with response to everolimus therapy, although confirmation in future studies is needed.


Even though cilostazol was assessed before in several models of atherosclerosis, so far its full systematic effect as a natural anti-inflammatory and anti-apoptotic mediator in the protection of liver damage and complication has not been fully clarified, which is the target of this study. For that purpose, we examined the protective effect of cilostazol (10 and 5 mg/kg, p.o. b.wt.) in an acute hepatic injury model by orally injecting it for 3 weeks prior to a single dose of TAA (300 mg/kg, i.p) injection. Ursodeoxycholic acid was used as a standard drug (50 mg/kg, p.o. b.wt.). After injection of thioacetamide by 48hr, rats were sacrificed. On the serum biochemical level, cilostazol ameliorated the thioacetamide consequence, where it presented a significant enhancement in the liver enzymes activities [Aspartate aminotransferase (AST) & Alanine aminotransferase (ALT)]. On the other hand, at the tissue level (Liver), it revealed a significant improvement in pro-inflammatory cytokines [Tumor necrosis factor alpha (TNF-alpha), Interleukin 1 beta (IL-1beta), Nuclear factor kappa B (NF-kB), NF-kB (P65/P50 nucleus translocation), caspase-3, cleaved caspase-3 & C-reactive protein (CRP)], redox level [Reduced glutathione (GSH) & Malondialdehyde (MDA)], histopathological findings, Reverse transcription polymerase chain reaction (RT-PCR) analysis (expression of TNF-alpha and NF-kB mRNA levels), and immunohistochemical reaction (caspase-3 & TNF-alpha). Obviously, the high dose of cilostazol (10 mg/kg, p.o. b.wt.) displayed a more pronounced effect than its lower one and nearly equal to ursodeoxycholic acid in the most of the parameters. These results give a new awareness into the hopeful molecular mechanisms by which cilostazol attenuates several factors participated in the progression of liver damage.

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