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#29036586   2017/10/16 Save this To Up

Epigenetic mechanisms underlie the crosstalk between growth factors and a steroid hormone.

Crosstalk between growth factors (GFs) and steroid hormones recurs in embryogenesis and is co-opted in pathology, but underlying mechanisms remain elusive. Our data from mammary cells imply that the crosstalk between the epidermal GF and glucocorticoids (GCs) involves transcription factors like p53 and NF-κB, along with reduced pausing and traveling of RNA polymerase II (RNAPII) at both promoters and bodies of GF-inducible genes. Essentially, GCs inhibit positive feedback loops activated by GFs and stimulate the reciprocal inhibitory loops. As expected, no alterations in DNA methylation accompany the transcriptional events instigated by either stimulus, but forced demethylation of regulatory regions broadened the repertoire of GF-inducible genes. We report that enhancers, like some promoters, are poised for activation by GFs and GCs. In addition, within the cooperative interface of the crosstalk, GFs enhance binding of the GC receptor to DNA and, in synergy with GCs, promote productive RNAPII elongation. Reciprocally, within the antagonistic interface GFs hyper-acetylate chromatin at unmethylated promoters and enhancers of genes involved in motility, but GCs hypoacetylate the corresponding regions. In conclusion, unmethylated genomic regions that encode feedback regulatory modules and differentially recruit RNAPII and acetylases/deacetylases underlie the crosstalk between GFs and a steroid hormone.

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#29036567   2017/10/16 Save this To Up

Extra-Pituitary Expressed FSH: Is It Physiologically Important?

Pituitary gonadotropes synthesize and secrete follicle-stimulating hormone (FSH). FSH is a heterodimer that consists of an α-and a β-subunit. The α - subunit is common to other pituitary and placental glycoprotein hormones and the β-subunit is the hormone/receptor specific subunit. Although the pituitary is the main tissue that accounts for circulating hormone, previous and recent reports indicate extra-pituitary sources of FSH production including mouse gonads, human stomach, prostate, umbilical cord vein endothelial cells, uterine myometrium, placenta and chicken abdominal adipose tissue. Whether extra-pituitary derived FSH exerts any physiologically significant actions is not known. In this review, we have comprehensively analyzed expression of mRNAs that encode mouse and human FSH subunits and also their corresponding expressed sequence tags in normal tissues, cancer cell lines and primary tumors by public database mining. We propose criteria to assess the significance of individual FSH subunit or FSH dimer expression as well as genetic approaches to unambiguously define the physiological relevance of extra-pituitary FSH expression.

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#29036458   2017/10/16 Save this To Up

Metabolic syndrome induces over expression of the human AT1R: a haplotype-dependent effect with implications on cardio-renal function.

The transcriptional regulation of the human AT1R gene in pathophysiologies, like the metabolic syndrome, is poorly understood. The human AT1R gene has polymorphisms in its promoter that can be arranged in two haplotypes. Variants -810T, -713T, -214A, and -153A always occur together (Hap-I) and variants -810A, -713G, -214C, and -153G form Hap-II. We have hypothesized that high fat diet will alter cellular transcriptional milieu and increase hAT1R gene expression in a haplotype-dependent manner. This will set up an AT1R-mediated feed-forward loop promoting inflammation, oxidative stress, and hypertension in Hap-I mice.

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#29036438   2017/10/16 Save this To Up

A selective sphingosine-1-phosphate receptor 1 agonist SEW-2871 aggravates gastric cancer by recruiting myeloid-derived suppressor cells.

The immune status of tumor microenvironment in gastric cancer is poorly understood, which limits the development of novel strategies in this field. Sphingosine-1-phosphate (S1P) acts as an immune modulator, but the role of S1P in gastric cancer is elusive. Here, we aim to investigate S1P receptor 1 (S1P1)-mediated effect of S1P in gastric cancer. We generated a xenograft mouse model and used SEW-2871, a S1P1 specific agonist to activate S1P1 signaling. Tumor-infiltrating lymphocytes (TILs) were isolated and analyzed using flow cytometry. Chemokine expression of tumor cells was evaluated using quantitative real-time polymerase chain reaction. Myeloid-derived suppressor cells (MDSCs) migration was assessed using Transwell chambers. SEW-2871 promoted tumor growth in our mouse model, and induced a higher level of MDSC and a reduced level of CD8+CD69+ T cells within tumor. Consistently, the anti-tumoral function of cytotoxic T lymphocytes was impaired in mice with SEW-2871 treatment. Additionally, SEW-2871 enhanced expression of several MDSC recruitment-associated chemokines (CXCL12, CXCL5 and CCL2) in tumor cells. These chemokines facilitated MDSC migration by interaction with CCR2, CXCR2 and CXCR4. S1P1 signaling promoted gastric cancer by enhancing chemokine expression in tumor cells and recruiting MDSC to tumor microenvironment, which impaired anti-tumoral function of TILs.

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#29036393   2017/10/16 Save this To Up

Angiotensin Receptor Expression and Vascular Endothelial Dysfunction in Obstructive Sleep Apnea.

Obstructive sleep apnea (OSA) is associated with vascular endothelial dysfunction (VED) in otherwise healthy patients. The role of renin-angiotensin system (RAS) in the OSA induced VED is not well understood.

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#29036356   2017/10/16 Save this To Up

Lipopolysaccharide promotes angiogenesis in mice model of HCC by stimulating hepatic stellate cell activation via TLR4 pathway.

Angiogenesis plays a key role in the progression of hepatocellular carcinoma (HCC). This study aimed to investigate whether lipopolysaccharide (LPS) could promote HCC angiogenesis and the role of hepatic stellate cell (HSC) in this process. In vivo orthotopic HCC model and the effect of LPS on HSC in vitro were studied. Our results demonstrated that LPS-induced HSC activation during the promotion of HCC growth and angiogenesis in mice. The LPS-TLR4 (Toll-like receptor 4) pathway in HSC is responsible for HCC angiogenesis. LPS-induced secretion of pro-angiogenic factors from HSC could promote endothelial cell migration and tubulogenesis. This study suggests that LPS acts with HSC in tumor stroma and promotes the secretion of pro-angiogenic factors that increase angiogenesis in HCC.

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#29036345   2017/10/16 Save this To Up

Phase II study of cabozantinib in patients with progressive glioblastoma: subset analysis of patients with prior antiangiogenic therapy.

Cabozantinib is a potent, multi-target inhibitor of hepatocyte growth factor receptor (MET) and vascular endothelial growth factor receptor-2 (VEGFR2). This open-label, phase II trial evaluated cabozantinib in patients with recurrent or progressive glioblastoma (GBM; NCT00704288).

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#29036337   2017/10/16 Save this To Up

A collection of mutants for CLE-peptide-encoding genes in Arabidopsis generated by CRISPR/Cas9 mediated gene targeting.

The ligand-receptor-mediated intercellular communication system plays important roles in coordinating developmental and physiological events in multicellular organisms. In plants, CLE peptides and their cognate receptors are thought to be involved in various aspects of the plant life cycle. Although the importance of this communication is broadly recognized, most CLE peptides are yet to be functionally characterized. A major problem in research on small signaling peptide-encoding genes is the limited number of loss-of-function mutants available due to their small gene size. CRISPR/Cas9-mediated gene targeting has the potential to overcome this problem, as it can be used to generate targeted mutations in essentially any gene, regardless of size. Here, we generated a series of mutants of CLE-peptide-encoding genes. Newly generated clv3 and cle40 mutants reproduced the expected mutant phenotypes in the shoot apical meristem and root meristem, respectively. Our results show that CRISPR/Cas9-mediated gene targeting is a powerful tool for genetic analyses, even of small genes. We also report a novel mutant for CLE44 (which is thought to encode a TDIF) and show that CLE44 contributes to vascular development. The bioresources presented here will be a powerful tool for further characterization of CLE peptides.

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#29036268   2017/10/16 Save this To Up

Breast Cancer Estrogen Receptor by Biological Generation: US Black & White Women, Born 1915-1979.

Evidence suggests contemporary population distributions of breast cancer estrogen receptor (ER) status may be shaped by earlier major societal events, such as the 1965 abolition of Jim Crow (legal racial discrimination in the US) and the Great Famine in China (1959-1961). We accordingly analyzed changes in ER status in relation to Jim Crow birth place among the 46,417 black and 339,830 white US-born non-Hispanic women in the 13 SEER Registry Group who were born between 1915 and 1979 and diagnosed (age 25-84, inclusive) between 1992-2012. We grouped the cases by birth cohort and quantified the rate of change using the haldane (which scales change in relation to biological generation). The % of ER+ cases rose by birth cohort (1915-1919 to 1975-1979) only among women diagnosed before age 55. Changes by biological generation were greater for black vs. white women, and among black women, were greatest among those born in Jim Crow vs. non-Jim Crow states, with this group the only one to exhibit high haldanes (>|0.3|, indicating high rate of change). Our study's analytic approach and findings underscore the need to consider history and societal context when analyzing breast cancer ER status and racial/ethnic inequities in its distribution.

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#29036202   2017/10/16 Save this To Up

Toxoplasma gondii induces FAK-Src-STAT3 signaling during infection of host cells that prevents parasite targeting by autophagy.

Targeting of Toxoplasma gondii by autophagy is an effective mechanism by which host cells kill the protozoan. Thus, the parasite must avoid autophagic targeting to survive. Here we show that the mammalian cytoplasmic molecule Focal Adhesion Kinase (FAK) becomes activated during invasion of host cells. Activated FAK appears to accompany the formation of the moving junction (as assessed by expression the parasite protein RON4). FAK activation was inhibited by approaches that impaired β1 and β3 integrin signaling. FAK caused activation of Src that in turn mediated Epidermal Growth Factor Receptor (EGFR) phosphorylation at the unique Y845 residue. Expression of Src-resistant Y845F EGFR mutant markedly inhibited ROP16-independent activation of STAT3 in host cells. Activation of FAK, Y845 EGFR or STAT3 prevented activation of PKR and eIF2α, key stimulators of autophagy. Genetic or pharmacologic inhibition of FAK, Src, EGFR phosphorylation at Y845, or STAT3 caused accumulation of the autophagy protein LC3 and LAMP-1 around the parasite and parasite killing dependent on autophagy proteins (ULK1 and Beclin 1) and lysosomal enzymes. Parasite killing was inhibited by expression of dominant negative PKR. Thus, T. gondii activates a FAK→Src→Y845-EGFR→STAT3 signaling axis within mammalian cells, thereby enabling the parasite to survive by avoiding autophagic targeting through a mechanism likely dependent on preventing activation of PKR and eIF2α.

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