Holmgaardwalther3348

Thyroid carcinoma (THCA) is a malignant tumor of the endocrine system. Previous studies have revealed the vital roles of microRNAs (miRNAs/miRs) in THCA procession. The present study aimed to explore the effects of miR‑15b‑5p on the progression of THCA and its targeting mechanism. read more The data of THCA and healthy samples were firstly collected from starbase2.0 and used to analyze the relationship of miR‑15b‑5p with THCA. Dual‑luciferase assay was performed to detect the direct interaction between miR‑15b‑5p and the predicted target gene GDP dissociation inhibitor 2 (GDI2). The effects of miR‑15b‑5p and GDI2 on the overall survival of patients with THCA were analyzed using Kaplan‑Meier analysis with log rank test. Cell Counting Kit‑8 and Transwell assays were conducted to assess the impacts of miR‑15b‑5p and GDI2 on the proliferation and invasion of THCA cells. Reverse transcription‑quantitative PCR and western blot analyses were performed to analyze the expression levels of the related miRNAs and proteins, respecease the understanding on the pathogenesis of THCA and provide novel candidates for THCA therapy.Intestinal malrotation in newborns often requires urgent surgical treatment, especially in the presence of volvulus. Therefore, early‑stage diagnosis is critical. In the present study, differentially expressed plasma microRNAs (miRNAs) were screened for in patients with intestinal malrotation using high‑throughput Illumina sequencing, and validated using reverse transcription‑quantitative PCR. Receiver operating characteristic curve (ROC) analysis was conducted to evaluate their specificity, sensitivity and assess their diagnostic value for intestinal malrotation. Bioinformatics analysis was performed to investigate the functions associated with the dysregulated miRNAs. A profile consisting of 28 differentially expressed plasma miRNAs was obtained, of which nine were verified to exhibit significantly altered expression. According to a ROC analysis, four of these could represent novel early‑stage, non‑invasive biomarkers for intestinal malrotation. Bioinformatics analysis demonstrated that the differentially expressed miRNAs were predominantly involved in 'metal ion transmembrane transporter activity' and 'calcium‑dependent protein binding', which may be related to the 'endocytosis' pathway. In conclusion, significantly differentially expressed plasma miRNAs were identified in congenital intestinal malrotation and their potential roles were described. These differentially expressed miRNAs may serve as biomarkers of intestinal malrotation and improve early diagnosis for this condition.Philadelphia chromosome‑positive acute lymphoblastic leukemia (Ph+ ALL) is regarded as a prognostically unfavorable subgroup, as this ALL subgroup has an increased risk of relapse/refractory disease. CD9, which belongs to the tetraspanin membrane proteins, is implicated in several pathological processes, including tumor progression. However, the role of CD9 in the pathogenesis of Ph+ ALL and the potential benefit of applying CD9‑targeted RNA interference strategies for treatment of Ph+ ALL require further investigation. The aim of the present study was to determine the effects of CD9 on leukemic cell progression and the efficacy of therapeutic agents in Ph+ ALL cells, in addition to assessing the in vitro anti‑leukemia activity of CD9‑targeted RNA interference in Ph+ ALL cells. In the present study, a lentiviral short hairpin RNA (shRNA) expression vector targeting CD9 gene in Ph+ ALL SUP‑B15 cells was constructed. The present results demonstrated that treatment of SUP‑B15 cells with lentiviral‑mediated shRNA against CD9 decreased CD9 mRNA and protein expression compared with the shControl cells transduced with a blank vector. In addition, CD9 knockdown could suppress cell proliferation, adhesion, migration and invasion, and promote apoptosis and the efficacy of chemotherapeutic drugs (such as vincristine, daunorubicin, cyclophosphamide and dexamethasone) and the tyrosine kinase inhibitor imatinib in SUP‑B15 cells. Furthermore, CD9 knockdown suppressed cell proliferation and promoted apoptosis in SUP‑B15 cells via a p53‑dependent pathway. These findings suggested that gene silencing of CD9 using a shRNA‑expressing lentivirus vector may provide a promising treatment for Ph+ ALL.The accumulation of β‑amyloid peptides (Aβ) in the brain is a hallmark of Alzheimer's disease (AD). Studies have indicated that ginsenoside Rg1, a primary component of ginseng (Panaxginseng), reduces brain Aβ levels in an AD model through peroxisome proliferator‑activated receptor γ (PPARγ), thereby regulating the expression of insulin‑degrading enzyme (Ide) and β‑amyloid cleavage enzyme 1 (Bace1), which are PPARγ target genes. However, the effects of ginsenoside Rg1 on PPARγ remain unclear. Since cyclin‑dependent kinase 5 (CDK5) mediates PPARγ phosphorylation in adipose tissue, this study aimed to investigate whether ginsenoside Rg1 regulates PPARγ target genes and reduces Aβ levels by inhibiting PPARγ phosphorylation through the CDK5 pathway. In the present study, a model of AD was established by treating primary cultured rat hippocampal neurons with Aβ1‑42. The cells were pretreatment with ginsenoside Rg1 and roscovitine, a CDK5‑inhibitor, prior to the treatment with Aβ1‑42. Neuronal apoptosis was detected using TUNEL staining. PPARγ phosphorylation and protein expression levels of PPARγ, CDK5, IDE, BACE1, amyloid precursor protein (APP) and Aβ1‑42 were measured by western blotting. The mRNA expression levels of PPARγ, CDK5, IDE, BACE1 and APP were assessed using reverse transcription‑quantitative PCR. The results of the present study demonstrated that in an AD model induced by Aβ1‑42, ginsenoside Rg1 significantly decreased CDK5 expression, inhibited PPARγ phosphorylation at serine 273, elevated IDE expression, downregulated BACE1 and APP expression, decreased Aβ1‑42 levels and attenuated neuronal apoptosis. The CDK5 inhibitor, roscovitine, demonstrated similar effects. These results suggest that ginsenoside Rg1 has neuroprotective properties and has potential for use in the treatment of AD.