No previous study investigated the anatomical changes of the scalp and hair follicles between tertiary androgenetic alopecia and severe alopecia areata using high-resolution magnetic resonance imaging (HR-MRI). This study aimed to explore the value of HR-MRI in assessing alopecia.
Esophageal cancer (EC) is the sixth most common cancer worldwide, and esophageal squamous-cell carcinoma (ESCC) accounts for more than 90% of ECs. We hypothesized that genetic factors might play an important role in ESCC carcinogenesis. We conducted a hospital-based case–control study to evaluate the association between two single nucleotide polymorphisms of decoy receptor 3 (DcR3), namely, rs2297441 G > A and rs2257440 T > C, on the ESCC risk. In all, 629 ESCC cases and 686 controls were included. Genotypes were determined using the ligation detection reaction method. When the DcR3 rs2297441 GG homozygote genotype was used as the reference group, the GA genotype showed no association with the ESCC risk (GA versus GG: adjusted OR = 1.11, 95% CI = 0.88–1.40, p = 0.396); similarly, even the TT genotype showed no association with the ESCC risk (AA versus GG: adjusted OR = 0.80, 95% CI = 0.55–1.18, p = 0.268). Logistic regression analyses revealed that the DcR3 rs2257440 T > C polymorphism was not associated with the ESCC risk. DcR3 rs2297441 G > A and DcR3 rs2257440 T > C polymorphisms may not contribute to the ESCC risk, and additional, larger studies are required to confirm our results.
Tumor invasion, metastasis, and recrudesce remain a considerable challenge in the treatment of gastric cancer (GC). Herein, we first identified that RBFOX3 (RNA binding protein fox-1 homolog 3) was significantly up-regulated in GC tissues and negatively linked to the survival rate of GC patients. RBFOX3 promoted cell division and cell cycle progression in vitro as well as in vivo. Furthermore, RBFOX3 increased cell invasion and migration ability. Interestingly, both the suppression of GC cell multiplication and invasion moderated by the silencing of RBFOX3 was rescued by HTERT up-regulation. Additionally, RBFOX3 augmented the resistance of GC cells to 5-fluorouracil (5-Fu) by repressing RBFOX3. Mechanistically, exogenous up-regulation of RBFOX3 triggered promoter activity and HTERT expression thereby enhancing the division and development of GC cells. Importantly, our findings revealed that RBFOX3 interacted with AP-2β to modulate the HTERT expression as demonstrated by co-immunoprecipitation analysis. In conclusion, our study indicates that high expression of RBFOX3 promotes GC progression and development but predicts worse prognosis by stimulating HTERT signaling. Moreover, the results suggest that the RBFOX3/AP-2β/HTERT pathway is a novel target for the development of therapeutic agents for the prevention and treatment of GC reappearance and metastasis.
ABSTRACT One hundred eighty pairs of tissues of esophageal squamous cell carcinoma (ESCC) were tested by the transcriptome sequencing in order to explore etiology factors. The chi‐square test and correlation analysis demonstrated that the relative expression levels of keratin 17 (KRT17) and collagen type I α1 chain (COL1A1) were significantly higher in EC with diabetes. Expression of KRT17 was correlated with blood glucose ( r = 0.204, p = 0.001) and tumor size ( r = −0.177, p = 0.038) in patients. COL1A1 correlated with age ( r = −0.170, p = 0.029) and blood glucose levels ( r = 0.190, p = 0.015). Experimental results of qRT‐PCR: KRT17 and COL1A1 genes were highly expressed in ESCC ( p < 0.05). When the two genes were used as a combination test, the positive detection rate of EC was 90.6%, and the ROC curve had greater power. The KRT17 and COL1A1 genes had the potential to be biomarkers for the diagnosis of ESCC.
Abstract LncRNA EIF3J-AS1 has shown to play an important regulatory role in a variety of tumor tissues, IGFB3 Gene is the target gene of LncRNA EIF3J-AS1, experimental studies shows that IGFB3 gene risk typing is associated with an increased risk of gastric cancer susceptibility of gastric cancer(GC),the relationship between LncRNA EIF3J-AS1 target IGFB3 Gene polymorphisms expression in GC patients is related. Methods : A case-controlled study was conducted, including 490 primary gastric cancers and 1476 normal controls. Targetscan, miRanda and other software are used to target and predict the genes and mirnas that lncRNA can bind to, and the expression correlation analysis is conducted, so as to construct the ceRNA network and speculate its regulation of gastric cancer expression. The target gene IGFB3 fragment was amplified in blood samples using PCR. Genotyping was performed using the snapshot method. Results : This rearch shows a signal pathway LncRNA EIF3J-AS1-IGFBP3, in IGFBP3 gene variants GA and GA + AA models, castric cancer can be decreased when in male subgroup and ≥ 61 years old subgroup, but during smoking and alcohol groups, gastic cancer risk is encreased. IGFBP3 gene is regulated by LncRNA EIF3J-AS1-miRNAs-IGFBP3 network, which could provide a potential drug target biomarker.
BACKGROUND: MicroRNAs regulating mRNA expression by targeting at mRNAs is known constructive in tumor occurrence, immune escape, and metastasis. OBJECTIVE: This research aims at finding negatively regulatory miRNA-mRNA pairs in esophageal squamous cell carcinoma (ESCC). METHODS: GENE expression data of The Cancer Genome Atlas (TCGA) and GEO database were employed in differently expressed RNA and miRNA (DE-miRNAs/DE-mRNAs) screening. Function analysis was conducted with DAVID-mirPath. MiRNA-mRNA axes were identified by MiRTarBase and TarBase and verified in esophageal specimen by real-time reverse transcription polymerase chain reaction (RT-qPCR). Receiver operation characteristic (ROC) curve and Decision Curve Analysis (DCA) were applied in miRNA-mRNA pairs predictive value estimation. Interactions between miRNA-mRNA regulatory pairs and immune features were analyzed using CIBERSORT. RESULTS: Combining TCGA database, 4 miRNA and 10 mRNA GEO datasets, totally 26 DE-miRNAs (13 up and 13 down) and 114 DE-mRNAs (64 up and 50 down) were considered significant. MiRTarBase and TarBase identified 37 reverse regulation miRNA-mRNA pairs, 14 of which had been observed in esophageal tissue or cell line. Through analysis of RT-qPCR outcome, miR-106b-5p/KIAA0232 signature was chosen as characteristic pair of ESCC. ROC and DCA verified the predictive value of model containing miRNA-mRNA axis in ESCC. Via affecting mast cells, miR-106b-5p/KIAA0232 may contribute to tumor microenvironment. CONCLUSIONS: The diagnostic model of miRNA-mRNA pair in ESCC was established. Their complex role in ESCC pathogenesis especially tumor immunity was partly disclosed.
Uremic cardiomyopathy (UCM) is a common complication in patients with chronic kidney disease (CKD) and an important risk factor for death. P-Cresyl sulfate (PCS) is a damaging factor in UCM, and Klotho is a protective factor. However, the molecular mechanisms of Klotho and PCS in UCM and the relationship between PCS and Klotho are unclear. In vitro, Klotho treatment inhibited PCS-induced cardiomyocyte hypertrophy and apoptosis by blocking mTOR phosphorylation and inhibiting DNA double-strand breaks (DSBs), respectively. Moreover, PCS increased SIRT6 protein ubiquitination and downregulated SIRT6 protein expression, while Klotho inhibited SIRT6 protein ubiquitination and upregulated SIRT6 protein expression. In a mouse model of 5/6 nephrectomy (5/6Nx)-induced UCM, the expression of Klotho in the kidney and serum was decreased, and the expression of SIRT6 protein in myocardial tissues was lower. PCS further reduced Klotho and SIRT6 expression, aggravated heart structure and function abnormalities, and increased myocardial cell apoptosis in UCM mice. Administration of Klotho protein inhibited the downregulation of SIRT6 protein expression and improved cardiac structure and function. Furthermore, serum PCS level was associated with the left ventricular mass (LVM) and left ventricular mass index (LVMI) in hemodialysis patients. In conclusion, the uremic toxin PCS injures cardiomyocytes via mTOR phosphorylation and DSBs, and Klotho antagonizes the damaging effects of PCS. Moreover, the SIRT6 protein plays an important role in UCM, and Klotho suppresses SIRT6 ubiquitination induced by PCS, further improves cardiac structure and function in UCM and exerts protective effects.
The development of noninvasive and sensitive detection methods for the early diagnosis and monitoring of bladder cancer is critical but challenging. Herein, an ultrasensitive electrochemiluminescence (ECL) immunosensor that uses Ru(bpy)32+-metal-organic framework (Ru-MOF) nanospheres and a DNA tetrahedral (TDN) probe was established for bladder cancer marker complement factor H-related protein (CFHR1) detection. The synthesized Ru(bpy)32+-metal-organic frameworks (Ru-MOFs) served as a linked substrate for immobilization of AuNPs and antibody (Ab2) to prepare the ECL signal probe (Ru-MOF@AuNPs-Ab2), exhibiting a stable and strengthened ECL emission. At the same time, the inherent advantages of TDN probes on the electrode as the capture probe (TDN-Ab1) improve the accessibility of targets to probes. In the presence of CFHR1, the signal probe Ru-MOF@AuNPs-Ab2 was modified on the electrode through immune binding, thereby obtaining an outstanding ECL signal. As expected, the developed ECL immunosensor exhibited splendid performance for CFHR1 detection in the range of 0.1 fg/mL to 10 pg/mL with a quite low detection limit of 0.069 fg/mL. By using the proposed strategy to detect CFHR1 from urine, it showed acceptable accuracy, which can effectively distinguish between bladder cancer patients and healthy samples. This work contributes to a novel, noninvasive, and accurate method for early clinical diagnosis of bladder cancer.
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