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Liraglutide suppresses proliferation and induces adipogenic differentiation of 3T3-L1 cells via the Hippo-YAP signaling pathway.

Liraglutide, as a glucagon-like peptide‑1 analogue, is used to treat type 2 diabetes mellitus and obesity. Previous findings have demonstrated the effects of liraglutide on adipogenesis; however, the underlying mechanism involved in this process remains to be elucidated. In the present study, to certify the effect of liraglutide on adipogenesis and explore the possible underlying mechanism involved in this process, preadipocyte 3T3‑L1 cells were cultured in adipocyte‑inducing medium and treated with liraglutide. Subsequently, the expression levels of the master transcription factors and adipocyte‑specific genes were measured by reverse transcription‑quantitative polymerase chain reaction and immunoblotting analysis. Lipid droplet production was detected by Oil red O staining. Cell proliferation was determined by a Cell Counting Kit-8 assay and cell immunofluorescence for Ki67, and apoptosis was assessed by flow cytometry. Next, the expression levels of the core components in the Hippo‑yes‑associated protein (YAP) signaling pathway as well as YAP‑specific target genes were measured. Finally, short interfering RNAs of mammalian ste20 kinase 1/2 (MST1/2), a key protein kinase in the Hippo‑YAP pathway, were used to determine whether liraglutide regulated adipogenic differentiation via the Hippo‑YAP pathway. It was demonstrated that liraglutide promoted adipogenic differentiation, suppressed proliferation, did not affect apoptosis of 3T3‑L1 cells and activated the Hippo‑YAP signaling pathway at the initial stage of adipogenesis. Silencing of MST1 counteracted the effect of increasing adipogenesis by liraglutide. These results suggested that liraglutide may activate the Hippo‑YAP signaling pathway leading to the inhibition of proliferation of preadipocyte 3T3‑L1 cells, and result in cells achieving transformation into mature adipocytes sooner. Taken together, the results of the present study may expand knowledge of the underlying mechanism of liraglutide facilitating adipogenesis, and may contribute to the development of GLP‑1 receptor agonists for weight loss and increased insulin sensitivity.

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INPP4B promotes cell survival via SGK3 activation in NPM1-mutated leukemia.

Acute myeloid leukemia (AML) with mutated nucleophosmin (NPM1) has been recognized as a distinct leukemia entity in the 2016 World Health Organization (WHO) classification. The genetic events underlying oncogenesis in NPM1-mutated AML that is characterized by a normal karyotype remain unclear. Inositol polyphosphate 4-phosphatase type II (INPP4B), a new factor in the phosphoinositide-3 kinase (PI3K) pathway-associated cancers, has been recently found a clinically relevant role in AML. However, little is known about the specific mechanistic function of INPP4B in NPM1-mutated AML.

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Discovery of a highly selective KIT kinase primary V559D mutant inhibitor for gastrointestinal stromal tumors (GISTs).

KIT kinase V559D mutation is the most prevalent primary gain-of-function mutation in Gastrointestinal Stromal Tumors (GISTs). Here we reported a highly selective KIT V559D inhibitor CHMFL-KIT-031, which displayed about 10-20 fold selectivity over KIT wt in the biochemical assay (IC50: 28 nM over 168 nM; Kd: 266 nM versus 6640 nM) and in cell (EC50: 176 nM versus 2000 nM for pY703) examination. It also displayed 15∼400-fold selectivity over other primary mutants such as L576P and secondary mutants including T670I, V654A (ATP binding pocket) as well as N822K and D816V (activation loop). In addition, it exhibited a selectivity S score (1) of 0.01 among 468 kinases/mutants in the KINOMEScan™ assay. CHMFL-KIT-031 showed potent inhibitory efficacy for KIT V559D mediated signaling pathways in cell and anti-tumor activity in vivo (Tumor Growth Inhibition: 68.5%). Its superior selectivity would make it a good pharmacological tool for further dissection of KIT V559D mediated pathology in the GISTs.

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Herbal formula YGJDSJ inhibits anchorage-independent growth and induces anoikis in hepatocellular carcinoma Bel-7402 cells.

Based on clinical medications and related studies, we established a Yang-Gan Jie-Du Sang-Jie (YGJDSJ) herbal formula for hepatocarcinoma treatment. In present study, we evaluated the anti-cancer potential of YGJDSJ on suspension-grown human hepatocellular carcinoma Bel-7402 cells.

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Oxidized phospholipids stimulate production of stem cell factor via NRF2-dependent mechanisms.

Receptor tyrosine kinase c-Kit and its ligand stem cell factor (SCF) regulate resident vascular wall cells and recruit circulating progenitors. We tested whether SCF may be induced by oxidized palmitoyl-arachidonoyl-phosphatidylcholine (OxPAPC) known to accumulate in atherosclerotic vessels. Gene expression analysis demonstrated OxPAPC-induced upregulation of SCF mRNA and protein in different types of endothelial cells (ECs). Elevated levels of SCF mRNA were observed in aortas of ApoE-/- knockout mice. ECs produced biologically active SCF because conditioned medium from OxPAPC-treated cells stimulated activation (phosphorylation) of c-Kit in naïve ECs. Induction of SCF by OxPAPC was inhibited by knocking down transcription factor NRF2. Inhibition or stimulation of NRF2 by pharmacological or molecular tools induced corresponding changes in SCF expression. Finally, we observed decreased levels of SCF mRNA in aortas of NRF2 knockout mice. We characterize OxPLs as a novel pathology-associated stimulus inducing expression of SCF in endothelial cells. Furthermore, our data point to transcription factor NRF2 as a major mediator of OxPL-induced upregulation of SCF. This mechanism may represent one of the facets of pleiotropic action of NRF2 in vascular wall.

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Human cytomegalovirus-encoded miR-UL112 contributes to HCMV-mediated vascular diseases by inducing vascular endothelial cell dysfunction.

Human cytomegalovirus (HCMV) infection has been linked to the pathogenesis of vasculopathy by inducing dysfunction of vascular cells such as endothelial cells. Hcmv-miR-UL112 is the most well-characterized HCMV-encoded microRNA occurring in the plasma of patients with cardiovascular diseases such as hypertension, while the specific underlying pathophysiological mechanisms are yet to be defined. The current study investigated the effect of hcmv-miR-UL112 on the growth and proliferation of human umbilical vascular endothelial cells (HUVECs); it might also be associated with signaling pathways. An adenovirus vector was designed and synthesized to stably express hcmv-miR-UL112 in HUVECs. Cell Counting Kit-8 results showed that ectopically expressed hcmv-miR-UL112 can significantly increase the proliferation of HUVECs (p < 0.05). Flow cytometry revealed that the S-phase fraction in the cell cycle analysis was raised significantly after overexpression of hcmv-miR-UL112 (p < 0.05). Gene expression profile analysis, using the microarray technology, revealed 303 up-regulated and 62 down-regulated genes in HUVECs by comparing the AD-hcmv-miR-UL112-infected and control groups (p < 0.05 and > 2 fold change). Kyoto Encyclopedia of Genes and Genomes and Reactome Pathway, chosen as the functional annotation categories, were affected by hcmv-miR-UL112 adenovirus vector. The significantly altered pathways mainly include the mitogen-activated protein kinase signaling pathway, cell adhesion molecules, chemokine signaling pathway, cytokine-cytokine receptor interaction, circadian rhythm-mammal, mineral absorption, protein processing in the endoplasmic reticulum, proximal tubule bicarbonate reclamation, vasopressin-regulated water reabsorption, and arachidonic acid metabolism. In conclusion, hcmv-miR-UL112 could serve as a potential biomarker, and the miRNA-mediated regulation of signaling pathways might play significant roles in the physiological effects of hcmv-associated diseases.

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Tormentic acid inhibits IL-1β-induced chondrocyte apoptosis by activating the PI3K/Akt signaling pathway.

Interleukin-1β (IL-1β) accelerates degradation of the cartilage matrix and induces apoptosis of chondrocytes. Tormentic acid (TA) is a triterpene isolated from the stem bark of the Vochysia divergens plant, which has been demonstrated to exert in vitro inhibitory activity against hepatocyte apoptosis. However, the effects of TA on IL‑1β‑induced apoptosis of human chondrocytes remain unclear. Therefore, the present study investigated the in vitro effects of TA on human osteoarthritic chondrocyte apoptosis cultivated in the presence of IL‑1β. Human chondrocytes were pretreated with or without various concentrations of TA and then co‑incubated in the absence or presence of IL‑1β for 24 h. Cell viability was determined using the MTT assay, and cell apoptosis was detected using a Nucleosome ELISA kit. Caspase‑3 activity was detected using a caspase‑3 colorimetric assay kit. The levels of B‑cell lymphoma 2 (Bcl‑2)‑associated X protein (Bax), Bcl‑2, phosphorylated (p)‑phosphoinositide 3‑kinase (PI3K), PI3K, p‑protein kinase B (Akt) and Akt were measured by western blotting. The results revealed that pretreatment with TA inhibited IL‑1β‑induced cytotoxicity and apoptosis in chondrocytes. In addition, TA pretreatment increased B‑cell lymphoma (Bcl)‑2 expression, and decreased caspase‑3 activity and Bax expressionin human chondrocytes. In addition, pretreatment with TA markedly increased the expression of p‑PI3K and p‑Akt in IL‑1β‑induced chondrocytes. Collectively, these results indicate that TA inhibits IL‑1β‑induced chondrocyte apoptosis by activating the PI3K/Akt signaling pathway. Therefore, TA may be considered a potential therapeutic target for the treatment of osteoarthritis.

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Tyrosine kinase inhibitor sensitive PDGFRΑ mutations in GIST: Two cases and review of the literature.

Gastrointestinal stromal tumors (GISTs) are rare mesenchymal malignancies of the gastrointestinal tract. Most GISTs harbor a c-KIT (80%) or a PDGFRα (10%) mutation that leads to constitutive activation of the tyrosine kinase receptor. Response to treatment with tyrosine kinase inhibitors (TKIs) is dependent on mutational status of the tumor. The most common mutation in PDGFRα, D842V, is known to be imatinib resistant. Almost all other PDGFRα mutations are imatinib sensitive. We describe two patients with a PDGFRα exon 18 mutated GIST responding to treatment with TKIs. One of these patients has a p.M844_S847 deletion, not previously described in relation with TKI treatment response. Mutations in circulating tumor DNA were detectable with digital droplet PCR in serial plasma samples taken during treatment and correlated with treatment response of both patients. Computer 3D-modeling of the PDGFRα kinase domain of these two variants revealed no direct interference in imatinib or sunitinib binding and no effect in its activity in contrast to the reported structure of the imatinib resistant D842V mutation. An overview is given of the literature regarding the evidence of patients with different PDGFRα mutated GISTs on response to TKIs. The findings emphasize the use of mutational analysis in GIST to provide patients personalized treatment. Detection of mutations in plasma is feasible and can provide real-time information concerning treatment response. We suggest to register GIST patients with these uncommon mutations in a prospective international database to understand the tumor biology and obtain more evidence of such mutations to predict treatment response.

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[SiRNA silencing Rsk2 gene expression inhibits proliferation and osteogenic differentiation of human periodontal ligament cells].

To study the effect of ribosomal S6 kinase (Rsk2) gene on proliferation and osteogenic differentiation of human periodontal ligament cells (hPDLCs) and underlying mechanism.

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Metformin Enhances the Differentiation of Dental Pulp Cells into Odontoblasts by Activating AMPK Signaling.

Metformin is a first-line drug for treating type 2 diabetes that regulates the differentiation of mesenchymal stem cells. Its effects on human dental pulp cells (DPCs) remain unknown. This study aimed to investigate the effects of metformin on the proliferation and differentiation of DPCs.

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