Impact of Social Support on Health Literacy Among People With Diabetes: A Cross-Sectional Study.

Aim: In recent years, the critical role of health literacy in diabetes management has become increasingly prominent. The aim of this study was to investigate the impact of social support on health literacy among patients with diabetes, to test the mediating role of self-efficacy and empowerment between social support and health literacy, and the moderating role of eHealth literacy.

Design: A cross-sectional study conducted between August 2023 and June 2024.

Comparison of metabolic syndrome prevalence and characteristics using five different definitions in China: a population-based retrospective study.

Background: Metabolic syndrome (MetS) is on the rise in developing countries and is characterized by a series of indications of metabolic disturbance. However, the prevalence of MetS varies under different definitions. The study aimed to compare five definitions of MetS in the China adult population, to explore their prevalence, characteristics and agreement.

N-glycosylation of CD82 at Asn157 is required for suppressing migration and invasion by reversing EMT via Wnt/β-catenin pathway in colon cancer.

CD82, a tetraspanin superfamily member, has been identified to be glycosylated at three specific residues (Asn129, Asn157, and Asn198). However, CD82 post-translational modification and its effect on colorectal cancer (CRC) metastasis remain unclear. Here, we constructed various deficient mutants of CD82 N-glycosylation in SW620 cells and demonstrated that the Asn157 site is necessary for CD82 glycosylation in CRC cells migration and LN-dependent adhesion in vitro.

Small extracellular ring domain is necessary for CD82/KAI1'anti-metastasis function.

The peptide mimicking small extracellular loop of CD82/KAI1 has been reported to inhibit tumor cell migration and metastasis. This provides an evidence that small extracellular loop domain should be important for the function of CD82/KAI1. In this paper, to investigate the structure basis for the function of EC1 mimic peptide, we systematically analyzed the effects of each amino acid residue in EC1 mimic peptide on its bioactivity.

The peptide mimicking small extracellular ring domain of CD82 inhibits tumor cell migration in vitro and metastasis in vivo.

Background: Tetraspanin KAI1/CD82, a tumor metastasis suppressor, has emerged as a promising molecular target for the management of metastatic disease. However, the peptide mimicking small extracellular ring domain (EC1) of CD82 has not been fully investigated for the function of inhibiting cell migration in vitro and tumor metastasis in vivo.

Methods: Different cancer cells were treated with EC1 mimic peptide in order to detect migration and invasion by the healing assay and transwell.

Gangliosides and CD82 inhibit the motility of colon cancer by downregulating the phosphorylation of EGFR at different tyrosine sites and signaling pathways.

Previous studies have shown that (GM3), a ganglioside, suppresses hepatoma cell motility and migration by inhibiting phosphorylation of EGFR and the activity of the PI3K/AKT signaling pathway. Therefore, the aim of the present study was to investigate whether the combined treatment of CD82 with gangliosides can exert a synergistic inhibitory effect on cell motility and migration. Epidermal growth factor receptor (EGFR) signaling was studied for its role in the mechanism through which CD82 and gangliosides synergistically inhibit the motility and migration of SW620 human colon adenocarcinoma cells.

The peptide mimicking small extracellular ring domain of CD82 inhibits epithelial-mesenchymal transition by downregulating Wnt pathway and upregulating hippo pathway.

We have previously demonstrated that the peptide mimicking small extracellular ring domain of CD82 (CD82EC1-mP) could inhibit tumor cell motility and metastasis. However, its acting mechanism is not understood. Here, we reported that the cell motility-inhibitory function of CD82EC1-mP was involved in the downregulation of epithelial-mesenchymal transition (EMT).

Ginsenoside protects against AKI via activation of HIF‑1α and VEGF‑A in the kidney‑brain axis.

Acute kidney injury (AKI) is characterized by abrupt kidney dysfunction. It results in remote organ dysfunction, including the brain. The underlying mechanism of the kidney‑brain axis in AKI and effective protective approaches remain unknown.

Exosomal protein CD82 as a diagnostic biomarker for precision medicine for breast cancer.

CD82, a member of the tetraspanin superfamily, has been proposed to exert its activity via tetra-transmembrane protein enriched microdomains (TEMs) in exosomes. The present study aimed to explore the potential of the exosome protein CD82 in diagnosing breast cancers of all stages and various histological subtypes in patients. The results strongly suggest that CD82 expression in breast cancer tissue was significantly lower than that in healthy and benign breast disease tissues.

The peptide mimicking small extracellular loop domain of CD82 inhibits tumor cell migration, adhesion and induces apoptosis by inhibiting integrin mediated signaling.

Within the extracellular domains of metastasis suppressor CD82, the large extracellular loop (EC2) has received much of the attention and its structure and function have been studied in detail. However, little attention has been given to the small extracellular loop (EC1 domain). To investigate the function role of EC1 in metastasis suppression of CD82, the peptide mimicking EC1 amino acid sequence (EC1-mP) was synthesized and its effect on cancer cells behavior was examined.

Core fucosylation of IgG B cell receptor is required for antigen recognition and antibody production.

Ag recognition and Ab production in B cells are major components of the humoral immune response. In the current study, we found that the core fucosylation catalyzed by α1,6-fucosyltransferase (Fut8) was required for the Ag recognition of BCR and the subsequent signal transduction. Moreover, compared with the 3-83 B cells, the coalescing of lipid rafts and Ag-BCR endocytosis were substantially reduced in Fut8-knockdown (3-83-KD) cells with p31 stimulation and then completely restored by reintroduction of the Fut8 gene to the 3-83-KD cells.

Ganglioside GM3 exerts opposite effects on motility via epidermal growth factor receptor and hepatocyte growth factor receptor-mediated migration signaling.

The ganglioside GM3 exerts its different effects via various growth factor receptors. The present study investigated and comparatively analyzed the opposing effects exerted by GM3 on the migration of mouse hepatocellular carcinoma Hepa1‑6 cells via epidermal growth factor receptor (EGFR) and hepatocyte growth factor receptor (HGFR/cMet). The results demonstrated that GM3 inhibited EGF‑stimulated motility, but promoted HGF‑stimulated motility of the Hepa1‑6 cells via phosphatidylinositol 3‑kinase/Akt‑mediated migration signaling.

Choline plasmalogens isolated from swine liver inhibit hepatoma cell proliferation associated with caveolin-1/Akt signaling.

Plasmalogens play multiple roles in the structures of biological membranes, cell membrane lipid homeostasis and human diseases. We report the isolation and identification of choline plasmalogens (ChoPlas) from swine liver by high performance thin layer chromatography (HPTLC) and high performance liquid chromatography (HPLC)/MS. The growth and viability of hepatoma cells (CBRH7919, HepG2 and SMMC7721) was determined following ChoPlas treatment comparing with that of human normal immortal cell lines (HL7702).

Cell recognition molecule L1 promotes embryonic stem cell differentiation through the regulation of cell surface glycosylation.

Cell recognition molecule L1 (CD171) plays an important role in neuronal survival, migration, differentiation, neurite outgrowth, myelination, synaptic plasticity and regeneration after injury. Our previous study has demonstrated that overexpressing L1 enhances cell survival and proliferation of mouse embryonic stem cells (ESCs) through promoting the expression of FUT9 and ST3Gal4, which upregulates cell surface sialylation and fucosylation. In the present study, we examined whether sialylation and fucosylation are involved in ESC differentiation through L1 signaling.

Laforin-malin complex degrades polyglucosan bodies in concert with glycogen debranching enzyme and brain isoform glycogen phosphorylase.

In Lafora disease (LD), the deficiency of either EPM2A or NHLRC1, the genes encoding the phosphatase laforin and E3 ligase, respectively, causes massive accumulation of less-branched glycogen inclusions, known as Lafora bodies, also called polyglucosan bodies (PBs), in several types of cells including neurons. The biochemical mechanism underlying the PB accumulation, however, remains undefined. We recently demonstrated that laforin is a phosphatase of muscle glycogen synthase (GS1) in PBs, and that laforin recruits malin, together reducing PBs.

Synergistic inhibition of cell migration by tetraspanin CD82 and gangliosides occurs via the EGFR or cMet-activated Pl3K/Akt signalling pathway.

The metastasis suppressor CD82/KAI-1, which is a member of the tetraspanin superfamily, has been proposed to exert its activity together with glycosphingolipids. However, the mechanism of CD82 inhibition has not been fully elucidated. The present study aimed to investigate the synergistic inhibition of cell migration by the tetraspanin CD82 and gangliosides and to correlate this inhibition with activation of epidermal growth factor receptor (EGFR) and hepatocyte growth factor receptor (HGFR/cMet) in Hepa1-6 cell lines, whose motility and migration is stimulated by epidermal growth factor (EGF) and hepatocyte growth factor (HGF) in vitro.

The cell adhesion molecule L1 regulates the expression of FGF21 and enhances neurite outgrowth.

L1 plays a role in neural development. However, it remains unclear how L1 plays this role. In the present study, we have shown extensive outgrowth of long neurites in cerebellar neurons after treatment with either L1 or L1 antibody.

Phosphorylation of cMet tyrosine residues in murine ascitic hepatic cancer cell lines with different lymph node metastatic potentials.

The aim of the present study was to determine the molecular mechanism by which the hepatocyte growth factor (HGF) receptor (cMet) regulates lymphatic metastasis in hepatocellular carcinoma. Mouse hepatoma ascites cell lines with different lymph node metastatic potentials, Hca‑F (high metastatic potential) and Hca‑P (low metastatic potential), were cultured in vitro. Cells were treated with HGF, fibronectin (FN) and laminin (LN), and the phosphorylated tyrosine residues of cMet and the activities of intracellular phospholipase Cγ/diacylglycerol/protein kinase C (PLCγ/DAG/PKC) and phosphoinositol‑3‑kinase/protein kinase B (PI3K/AKT) signaling pathways were analyzed comparatively in the two cell lines using western blot analysis and migration assays.

Ganglioside GM3 promotes HGF-stimulated motility of murine hepatoma cell through enhanced phosphorylation of cMet at specific tyrosine sites and PI3K/Akt-mediated migration signaling.

Ganglioside GM3 plays a well-documented and important role in the regulation of tumor cell proliferation, invasion, and metastasis by modulating tyrosine kinase growth factor receptors. However, the effect of GM3 on the hepatocyte growth factor receptor (HGFR, cMet) has not been fully delineated. In the current study, we investigated how GM3 affects cMet signaling and HGF-stimulated cell motility and migration using three hepatic cancer cell lines of mouse (Hca/A2, Hca/16A3, and Hepa1-6).

Laforin prevents stress-induced polyglucosan body formation and Lafora disease progression in neurons.

Glycogen, the largest cytosolic macromolecule, is soluble because of intricate construction generating perfect hydrophilic-surfaced spheres. Little is known about neuronal glycogen function and metabolism, though progress is accruing through the neurodegenerative epilepsy Lafora disease (LD) proteins laforin and malin. Neurons in LD exhibit Lafora bodies (LBs), large accumulations of malconstructed insoluble glycogen (polyglucosans).

Protein aggregation of SERCA2 mutants associated with Darier disease elicits ER stress and apoptosis in keratinocytes.

Mutations in sarcoplasmic/endoplasmic reticulum calcium ATPase 2 (SERCA2) underlie Darier disease (DD), a dominantly inherited skin disorder characterized by loss of keratinocyte adhesion (acantholysis) and abnormal keratinization (dyskeratosis) resulting in characteristic mucocutaneous abnormalities. However, the molecular pathogenic mechanism by which these changes influence keratinocyte adhesion and viability remains unknown. We show here that SERCA2 protein is extremely sensitive to endoplasmic reticulum (ER) stress, which typically results in aggregation and insolubility of the protein.

Over-expression of pemt2 into rat hepatoma cells contributes to the mitochondrial apoptotic pathway.

We previously established a line of phosphatidylethanolamine N-methyltransferase 2 (pemt2) -stably transfected CBRH-7919 hepatoma cells, and showed that pemt2 over-expression inhibited cell proliferation and induced apoptosis. This study was aimed to further elucidate the cellular mechanisms leading to this apoptosis in these cells. Fatty acid compositions of phosphatidylcholine (PC) in pemt2 over-expressed cells and control cells, and the location of PC synthesized by PEMT2 pathway were analyzed with lipid extraction, high-performance thin layer chromatography, high-performance gas chromatography (HPGC), and [(3)H]-ethanolamine tracing.

LeY oligosaccharide upregulates DAG/PKC signaling pathway in the human endometrial cells.

LeY oligosaccharide is stage specifically expressed by the embryo and uterine endometrium, and it plays important roles in embryo implantation. In addition to participating in the recognition and adhesion on fetal-maternal interface, LeY potentially regulates the expression of some implantation-related factors. However, it remains elusive whether it can mediate the involved signaling pathway.

[Effects of lipid rafts on signal transmembrane transduction mediated by c-Met].

Objective: To study the effects of lipid rafts on cell signal transmembrane transduction mediated by c-Met.

Methods: After HepG2Cells were treated with MbCD to disrupt the lipid rafts and were treated with artificial recombination hepatocyte growth factor to activate c-Met, the activities of PLCr1/PKC, PI3K/Akt and MAPK signaling pathways in HepG2 cells were analyzed using Western blot.

Results: (1) After disruption of lipid rafts with MbCD, phosphorylation of PLCr1 decreased by 35% (P = 0.