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Source: Journal of Molecular Medicine
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Total 44 results found since Jan 2013.
Coexpression of FOXK1 and vimentin promotes EMT, migration, and invasion in gastric cancer cells
We report that FOXK1 synergizes with vimentin to promote GC invasion and metastasis via the induction of epithelial-mesenchymal transition (EMT). We showed that higher expression levels of FOXK1 were significantly associated with GC development. FOXK1 can physically interact with and stabilize vimentin. Moreover, a positive correlation between the expression of FOXK1 and vimentin was found in GC cells. Higher expression levels of these two proteins were significantly associated with differentiation, lymph node metastasis, AJCC stage, and poorer prognosis. Furthermore, the coexpression of FOXK1 and vimentin enhances cell me...
Source: Journal of Molecular Medicine - November 27, 2018 Category: Molecular Biology Source Type: research
Interleukin-23 receptor signaling mediates cancer dormancy and radioresistance in human esophageal squamous carcinoma cells via the Wnt/Notch pathway
In this study, we investigated the effect of extracellular IL-23 in IL-23 receptor-positive (IL-23R+) esophageal squamous cell carcinoma (ESCC) and explored the mechanisms underlying this effect. We analyzed ESCC tumor tissues by immunohistochemical and immunofluorescence staining and found that IL-23, which was highly expressed, co-localized with Oct-4A in IL-23R+ ESCC cells. In addition, IL-23 treatment significantly increased the accumulation of CD133+ cells and activated the Wnt and Notch signaling pathways in CD133−IL-23R+ ESCC cell lines. Consistently, CD133−IL-23R+ cells pretreated with IL-23 showed stronger ant...
Source: Journal of Molecular Medicine - November 27, 2018 Category: Molecular Biology Source Type: research
Inhibition of YAP with siRNA prevents cartilage degradation and ameliorates osteoarthritis development
AbstractThe Hippo/YAP signaling pathway is important for mediating organ size and tissue homeostasis, but its role in osteoarthritis (OA) remains unclear. We aimed to investigate the role of Hippo/YAP signaling pathway in OA development. YAP expression in OA cartilage was assessed by immunohistochemistry, RT-qPCR, and Western blotting. The effects of YAP overexpression or knockdown on gene expression related to chondrocyte hypertrophy induced by IL-1 β were examined. The in vivo effects of YAP inhibition were studied. Subchondral bone was analyzed by micro-CT. YAP was increased in mice and human OA articular cartilage and...
Source: Journal of Molecular Medicine - November 21, 2018 Category: Molecular Biology Source Type: research
Trichostatin A, a histone deacetylase inhibitor, induces synergistic cytotoxicity with chemotherapy via suppression of Raf/MEK/ERK pathway in urothelial carcinoma
In conclusion, TSA elicits a synergistic cytotoxic response in combination with chemotherapy via targeting the Raf/MEK/ERK pathway. TSA elicits synergistic cytotoxic response in combination with three DNA-damaging drugs (cisplatin, gemcitabine, and doxorubicin). Activated Raf/MEK/ERK pathway is involved in chemoresistant mechanism of UC. Combining chemotherapeutic agents with HDAC inhibitor (TSA) or with targeting Raf/MEK/ERK pathway is promising to c ircumvent chemoresistance in UCs.
Source: Journal of Molecular Medicine - October 4, 2018 Category: Molecular Biology Source Type: research
High-fat diet consumption reduces hepatic folate transporter expression via nuclear respiratory factor-1
AbstractFolate is an essential micronutrient for biological function. The liver, a primary organ for folate metabolism and storage, plays an important role in folate homeostasis. Proton-coupled folate transporter (PCFT) and reduced folate carrier (RFC) are the major folate transporters responsible for folate uptake at basolateral membrane of hepatocytes. Low serum folate levels are frequently associated with obesity. We investigated the mechanism that regulated folate status in a mouse model with diet-induced obesity. Mice (C57BL/6J) were fed a high-fat diet (60% kcal fat) for 8 weeks. Mice displayed increased hepatic li...
Source: Journal of Molecular Medicine - September 4, 2018 Category: Molecular Biology Source Type: research
NLRP3 deficiency accelerates pressure overload-induced cardiac remodeling via increased TLR4 expression
AbstractNLRP3, a member of the nucleotide-binding oligomerization domain (NOD)-like receptor family, is involved in cardiac inflammation. However, the functional role of NLRP3 in cardiac remodeling is not clear. To investigate the roles of NLRP3 in pressure overload-induced cardiac remodeling, NLRP3 knockout and wild-type mice were subjected to aortic banding to induce cardiac remodeling. The data showed that NLRP3 expression was downregulated in the remodeling process. NLRP3 deficiency accelerated cardiac hypertrophy, fibrosis, and inflammation responses with deteriorating cardiac dysfunction in the pressure overload-indu...
Source: Journal of Molecular Medicine - August 29, 2018 Category: Molecular Biology Source Type: research
Bispecific therapeutic aptamers for targeted therapy of cancer: a review on cellular perspective
AbstractAptamers (Aps), as short single-strand nucleic acids, can bind to their corresponding molecular targets with the high affinity and specificity. In comparison with the monoclonal antibodies (mAbs) and peptides, unique physicochemical and biological characteristics of Aps make them excellent targeting agents for different types of cancer molecular markers (CMMs). Much attention has been paid to the Ap-based multifunctional chimeric and therapeutic systems, which provide promising outcomes in the targeted therapy of various formidable diseases, including malignancies. In the Ap-based chimeric systems, a targeting Ap i...
Source: Journal of Molecular Medicine - July 28, 2018 Category: Molecular Biology Source Type: research
Co-targeting PLK1 and mTOR induces synergistic inhibitory effects against esophageal squamous cell carcinoma
In this study, we found that suppression of PLK1 by specific siRNA or inhibitor attenuated mTOR activity in ESCC cells. Phosphorylated S6, a downstream effector of mTOR signaling, was significantly correlated with overexpression of PLK1 in a subset of ESCC. These data suggest that PLK1 activates mTOR signaling in vitro and in vivo. More importantly, the mTOR inhibitor rapamycin synergized with PLK1 inhibitor BI 2536 to inhibit ESCC cell proliferation in culture and in mice. Notably, combined treatment with BI 2536 and rapamycin produced more potent inhibitory effects on the activation of S6 and AKT than either alone. Furth...
Source: Journal of Molecular Medicine - June 29, 2018 Category: Molecular Biology Source Type: research
MicroRNA-210-mediated proliferation, survival, and angiogenesis promote cardiac repair post myocardial infarction in rodents
AbstractAn innovative approach for cardiac regeneration following injury is to induce endogenous cardiomyocyte (CM) cell cycle re-entry. In the present study, CMs from adult rat hearts were isolated and transfected with cel-miR-67 (control) and rno-miR-210. A significant increase in CM proliferation and mono-nucleation were observed in miR-210 group, in addition to a reduction in CM size, multi-nucleation, and cell death. When compared to control, β-catenin and Bcl-2 were upregulated while APC (adenomatous polyposis coli), p16, and caspase-3 were downregulated in miR-210 group. In silico analysis predicted cell cycle inhi...
Source: Journal of Molecular Medicine - September 25, 2017 Category: Molecular Biology Source Type: research
Sequential combination of docetaxel with a SHP-1 agonist enhanced suppression of p-STAT3 signaling and apoptosis in triple negative breast cancer cells
AbstractTriple negative breast cancer (TNBC) is an aggressive cancer for which prognosis remains poor. Combination therapy is a promising strategy for enhancing treatment efficacy. Blockade of STAT3 signaling may enhance the response of cancer cells to conventional chemotherapeutic agents. Here we used a SHP-1 agonist SC-43 to dephosphorylate STAT3 thereby suppressing oncogenic STAT3 signaling and tested it in combination with docetaxel in TNBC cells. We first analyzed messenger RNA (mRNA) expression of SHP-1 gene (PTPN6) in a public TNBC dataset (TCGA) and found that higher SHP-1 mRNA expression is associated with better ...
Source: Journal of Molecular Medicine - June 4, 2017 Category: Molecular Biology Source Type: research
HuR mediates motility of human bone marrow-derived mesenchymal stem cells triggered by sphingosine 1-phosphate in liver fibrosis
AbstractSphingosine 1-phosphate (S1P) participates in migration of bone marrow (BM)-derived mesenchymal stem cells (BMSCs) toward damaged liver via upregulation of S1P receptor 3 (S1PR3) during mouse liver fibrogenesis. But, the molecular mechanism is still unclear. HuR, as an RNA-binding protein, regulates tumor cell motility. Here, we examined the role of HuR in migration of human BMSCs (hBMSCs) in liver fibrosis. Results showed that HuR messenger RNA (mRNA) level was increased in human or mouse fibrotic livers, and correlated with S1PR3 mRNA expression. Using immunofluorescence, we found that HuR mainly localized in the...
Source: Journal of Molecular Medicine - August 19, 2016 Category: Molecular Biology Source Type: research
Fis1 depletion in osteoarthritis impairs chondrocyte survival and peroxisomal and lysosomal function
This study represents the first functional study of Fis1 with its pathological relevance to OA. Our data suggest a new target for controlling cartilage-degenerative diseases, such as OA.Key messageFis1 suppression in OA chondrocytes induces accumulation and inhibition of lysosomes.Fis1 suppression alters miRNAs, especially those implicated in lysosomal regulation.Lysosomal destruction results in chondrocyte apoptosis and suppression of autophagy.Fis1 depletion in zebrafish causes lysosome accumulation, mitochondrial dysfunction, and peroxisome reduction.This is the first functional study of Fis1 and its pathological relevance to OA.
Source: Journal of Molecular Medicine - August 5, 2016 Category: Molecular Biology Source Type: research
Resveratrol inhibits renal interstitial fibrosis in diabetic nephropathy by regulating AMPK/NOX4/ROS pathway
In this study, we first demonstrated that high glucose could induce renal fibroblast (NRK-49F) cell proliferation and activation to myofibroblasts, accompanied by a significant increase in the intracellular levels of reactive oxygen species (ROS) derived from nicotinamide adenine dinucleotide phosphate oxidase 4 (NOX4). ROS-mediated ERK1/2 activation was found to play a crucial role in high glucose-induced fibroblast proliferation and activation. Resveratrol, like the NOX4-targeting small interfering RNA (siRNA), markedly inhibited high glucose-induced fibroblast proliferation and activation by reducing NOX4-derived ROS pr...
Source: Journal of Molecular Medicine - August 3, 2016 Category: Molecular Biology Source Type: research
