SCF Complex Targets Interleukin-17 Receptor A for Ubiquitin-Proteasome-Mediated Degradation.

Interleukin-17 (IL-17) is a pro-inflammatory cytokine that participates in innate and adaptive immune responses and plays an important role in host defense, autoimmune diseases, tissue regeneration, metabolic regulation, and tumor progression. Post-translational modifications (PTMs) are crucial for protein function, stability, cellular localization, cellular transduction, and cell death. However, PTMs of IL-17 receptor A (IL-17RA) have not been investigated.

Defect of IL17 Signaling, but Not Centrinone, Inhibits the Development of Psoriasis and Skin Papilloma in Mouse Models.

Patients with psoriasis tend to develop skin cancer, and the hyperproliferation of the epidermis is a histopathological hallmark of both psoriasis and cutaneous squamous cell carcinoma (SCC), indicating that they may share pathogenic mechanisms. Interleukin-17 (IL17) stimulates the proliferation of the epidermis, leading to psoriasis. Overexpression of Polo-like kinase 4 (PLK4), which controls centriole duplication, has been identified in SCC, which also shows the hyperproliferation of keratinocytes.

expression defines a subpopulation of cells with chondrogenic potentials in E12.5 mouse embryonic limbs.

Growth differentiation factor 5 () and doublecortin () genes are both expressed in joint interzone cells during synovial joint development. In this study, we re-analyzed the single cell RNA-sequencing data (Gene Expression Omnibus GSE151985) generated from cells of mouse knee joints at embryonic stages of E12.5, E13.

CDK4/6 inhibitor palbociclib reduces inflammation in lupus-prone mice.

Lupus is an autoimmune inflammatory disease that affects multiple organs. Cyclin-dependent kinases (CDKs) have been associated with inflammation. The objective of this study was to explore the effects of palbociclib (a CDK4/6 inhibitor) on inflammation in a lupus-prone MRL-lpr mouse model.

Intra-arterial injection to create bone metastasis of prostate cancer in mice.

Human prostate cancer often metastasizes to the bone, but the mechanisms are not quite clear. The difficulties in studying the biology of bone metastasis are due to lack of animal models with high frequency of bone metastases. In the present study, we tested two intra-arterial injection methods, i.

Th17 cells promote tumor growth in an immunocompetent orthotopic mouse model of prostate cancer.

Interleukin-17 (IL-17) has been demonstrated to promote development of a variety of cancers including prostate cancer in genetically modified mouse models. IL-17 is the main product secreted by T helper 17 (Th17) cells. A recent study has shown that Th17 cells and related genes are upregulated in human prostate cancers.

PD-L1 instead of PD-1 status is associated with the clinical features in human primary prostate tumors.

Immunotherapy targeting programmed cell death protein 1 (PD-1)/programmed cell death-ligand 1 (PD-L1) has shown efficacy in a variety of solid tumors. However, prostate cancer has often been a non-responder to anti-PD-1/PD-L1 therapies. The objective of this study was to determine PD-1 and PD-L1 expression status and its correlation with clinical features of the patients.

Interleukin-17 Promotes Migration and Invasion of Human Cancer Cells Through Upregulation of MTA1 Expression.

Interleukin-17 (IL-17) has been shown to promote development of prostate, colon, skin, lung, breast, and pancreatic cancer. The purpose of this study was to determine if IL-17 regulates MTA1 expression and its biological consequences. Human cervical cancer HeLa and human prostate cancer DU-145 cell lines were used to test if IL-17 regulates metastasis associated 1 (MTA1) mRNA and protein expression using quantitative reverse transcription-polymerase chain reaction and Western blot analysis, respectively.

Organoid culture of human prostate cancer cell lines LNCaP and C4-2B.

Organoids mimic the architecture and functions of a small organ. Organoid culture technique has been rapidly accepted by all research communities during the past decade to study stem cells, organ development and function, and patient-specific diseases. A protocol for organoid culture of human and mouse prostate epithelial and cancer tissues has been reported.

Targeting Th17-IL-17 Pathway in Prevention of Micro-Invasive Prostate Cancer in a Mouse Model.

Background: Chronic inflammation has been associated with the development and progression of human cancers including prostate cancer. The exact role of the inflammatory Th17-IL-17 pathway in prostate cancer remains unknown. In this study, we aimed to determine the importance of Th17 cells and IL-17 in a Pten-null prostate cancer mouse model.

Hyperinsulinemia enhances interleukin-17-induced inflammation to promote prostate cancer development in obese mice through inhibiting glycogen synthase kinase 3-mediated phosphorylation and degradation of interleukin-17 receptor.

Interleukin-17 (IL-17) plays important roles in inflammation, autoimmune diseases, and some cancers. Obese people are in a chronic inflammatory state with increased serum levels of IL-17, insulin, and insulin-like growth factor 1 (IGF1). How these factors contribute to the chronic inflammatory status that promotes development of aggressive prostate cancer in obese men is largely unknown.

miR-134 Modulates the Proliferation of Human Cardiomyocyte Progenitor Cells by Targeting Meis2.

Cardiomyocyte progenitor cells play essential roles in early heart development, which requires highly controlled cellular organization. microRNAs (miRs) are involved in various cell behaviors by post-transcriptional regulation of target genes. However, the roles of miRNAs in human cardiomyocyte progenitor cells (hCMPCs) remain to be elucidated.

Interleukin-17 Indirectly Promotes M2 Macrophage Differentiation through Stimulation of COX-2/PGE2 Pathway in the Cancer Cells.

Purpose: Interleukin-17 (IL-17) is a proinflammatory cytokine that plays important roles in inflammation, autoimmunity, and cancer. The purpose of this study was to determine if IL-17 indirectly regulates macrophage differentiation through up-regulation of cyclooxygenase-2 (COX-2) expression in the cancer cell lines.

Materials And Methods: Human cervical cancer HeLa, human lung cancer A549, and mouse prostate cancer Myc-CaP/CR cell lines were treated with recombinant IL-17; Western blot analysis, enzyme-linked immunosorbent assay, and quantitative real-time polymerase chain reaction analysis were utilized to examine the cellular responses.

Doublecortin may play a role in defining chondrocyte phenotype.

Embryonic development of articular cartilage has not been well understood and the role of doublecortin (DCX) in determination of chondrocyte phenotype is unknown. Here, we use a DCX promoter-driven eGFP reporter mouse model to study the dynamic gene expression profiles in mouse embryonic handplates at E12.5 to E13.

Insulin and IGF1 enhance IL-17-induced chemokine expression through a GSK3B-dependent mechanism: a new target for melatonin's anti-inflammatory action.

Obesity is a chronic inflammation with increased serum levels of insulin, insulin-like growth factor 1 (IGF1), and interleukin-17 (IL-17). The objective of this study was to test a hypothesis that insulin and IGF1 enhance IL-17-induced expression of inflammatory chemokines/cytokines through a glycogen synthase kinase 3β (GSK3B)-dependent mechanism, which can be inhibited by melatonin. We found that insulin/IGF1 and lithium chloride enhanced IL-17-induced expression of C-X-C motif ligand 1 (Cxcl1) and C-C motif ligand 20 (Ccl20) in the Gsk3b(+/+) , but not in Gsk3b(-/-) mouse embryonic fibroblast (MEF) cells.

Glyphosate and AMPA inhibit cancer cell growth through inhibiting intracellular glycine synthesis.

Glycine is a nonessential amino acid that is reversibly converted from serine intracellularly by serine hydroxymethyltransferase. Glyphosate and its degradation product, aminomethylphosphonic acid (AMPA), are analogs to glycine, thus they may inhibit serine hydroxymethyltransferase to decrease intracellular glycine synthesis. In this study, we found that glyphosate and AMPA inhibited cell growth in eight human cancer cell lines but not in two immortalized human normal prostatic epithelial cell lines.

Comparison of the tendon damage caused by four different anchor systems used in transtendon rotator cuff repair.

Objectives. The objective of this study was to compare the damage to the rotator cuff tendons caused by four different anchor systems. Methods.

Interleukin-17 and prostaglandin E2 are involved in formation of an M2 macrophage-dominant microenvironment in lung cancer.

Introduction: Tumor-associated macrophages (TAMs) are divided into M1 and M2 macrophages. M1 macrophages inhibit tumor growth, whereas M2 macrophages promote tumor growth and metastasis. The aim of this study was to examine the possible causes leading to the formation of an M2-macrophage-dominant tumor microenvironment in non-small-cell lung cancer.

Interleukin-17 promotes formation and growth of prostate adenocarcinoma in mouse models.

The contributions of interleukin (IL)-17 to cancer remain unclear and somewhat controversial. We took a genetic approach to explore its role in prostate cancers by interbreeding IL-17 receptor C (IL-17RC)-deficient mice with mice that are conditionally mutant for PTEN, one established preclinical model for prostate cancer. Mice that were IL-17RC-deficient (IL-17RC(-)) displayed prostates that were smaller than mice that maintained IL-17RC expression (IL-17RC(+)).

LNCaP prostate cancer cells with autocrine interleukin-6 expression are resistant to IL-6-induced neuroendocrine differentiation due to increased expression of suppressors of cytokine signaling.

Background: Neuroendocrine differentiation (NED) is one of the mechanisms underlying development of castration-resistant prostate cancer (CRPC). In this study, we investigated IL-6-induced NED in two LNCaP sublines.

Methods: LNCaP-S17, an LNCaP subline that secretes IL-6, and LNCaP-C3, a control subline that does not express IL-6, were analyzed for IL-6-induced NED, activation of JAK2 and STAT3 pathways, and expression of IL-6/IL-6R signaling proteins and downstream target genes.

Interleukin-17 Induces Expression of Chemokines and Cytokines in Prostatic Epithelial Cells but Does Not Stimulate Cell Growth In Vitro.

Background: Interleukin-17 (IL-17A) expression is increased in prostate cancer. This study investigated the expression of IL-17A receptor C (IL-17RC) in prostatic intraepithelial neoplasia (PIN) lesions and the effects of IL-17A on prostatic epithelial cells in studies.

Methods: IL-17RC expression in human and rodent prostate tissues was detected by immunohistochemistry.

Supraphysiologic temperature enhances cytotoxic effects of bupivacaine on bovine articular chondrocytes in an in vitro study.

Purpose: The purpose of this study was to determine the effects of temperature or 0.25% bupivacaine treatment in combination with supraphysiologic temperatures on chondrocyte viability.

Methods: Bovine articular chondrocytes in suspension culture were treated with phosphate-buffered saline solution at 20°C, 37°C, 40°C, 42°C, 45°C, 47°C, and 50°C for 15, 30, and 60 minutes or with phosphate-buffered saline solution at 37°C, 45°C, and 50°C for 30 and 60 minutes followed by 0.

Expression of doublecortin reveals articular chondrocyte lineage in mouse embryonic limbs.

The doublecortin (Dcx) gene encodes a microtubule-binding protein that was originally found in immature neurons. In this study, we used two mouse strains that express reporter genes (LacZ and enhanced green fluorescence protein, respectively) driven by the endogenous Dcx promoter. We found that Dcx was expressed in the mesenchymal cells in the mouse embryonic limb buds.

Is chemical incompatibility responsible for chondrocyte death induced by local anesthetics?

Background: Chondrolysis associated with intra-articular administration of local anesthetics has been attributed to chondrocyte death induced by the local anesthetics. The mechanism of how the local anesthetics cause chondrocyte death is not clear.

Purpose: This study was conducted to determine whether and how the local anesthetics cause chondrocyte death.