Lyngehunter4838

Long non-coding RNAs (lncRNAs) and their N6-methyladenosine (M6A) modifications are involved in cancer occurrence and development.

lncRNA M6A modification in colorectal cancer (CRC) was comprehensively analyzed for the first time.

M6A levels of lnRNAs in CRC tissues were higher than those in tumor-adjacent normal tissues. A total of 8,332 M6A peaks were detected in 6,690 lncRNAs in CRC tissues. Approximately 91% of the modified lncRNAs had unique M6A modification peaks. A total of 383 lncRNAs were differentially methylated in CRC, of which 48.24% had a length of 1-1,000 bp. Most of these were located on chromosomes 1, 2, 7, 11, 16 and 19; 42.3% were within a sense-overlapping exon. RNA sequencing identified 163 differentially expressed lncRNAs in CRC. GO and KEGG analyses revealed that genes near differentially-methylated or -expressed lncRNAs were associated with CRC occurrence and development. Methylation was positively correlated with lncRNA expression levels in CRC and tumor-adjacent normal tissues. More unmethylated than M6A methylated lncRNA molecules were detected. A competing endogenous RNA (ceRNA) and lncRNA-mRNA expression-regulation network revealed a regulatory relationship between lncRNAs, microRNAs (miRNAs), and mRNAs.

The findings may help improve our understanding of lncRNA function in colorectal cancer.

The findings may help improve our understanding of lncRNA function in colorectal cancer.In this study, we examined data from 69 gout patients and 1,455 non-gout controls using a MethylationEPIC BeadChip assay and Illumina HiSeq platform to identify lineage-specific epigenetic alterations and associated genetic factors that contributed to gouty inflammation. Cell lineage-specific differentially methylated sites were identified using CellDMC after adjusting for sex, age, alcohol drinking, smoking status, and smoking history (total pack-years). Different cell lineages displayed distinct differential methylation. Ingenuity Pathway Analysis and NetworkAnalyst indicated that many differential methylated sites were associated with interleukin-1β expression in monocytes. On the UCSC Genome Browser and WashU Epigenome Browser, metabolic trait, cis-methylation quantitative trait loci, genetic, and functional annotation analyses identified nine methylation loci located in interleukin-1β-regulating genes (PRKCZ, CIDEC, VDAC1, CPT1A, BIRC2, BRCA1, STK11, and NLRP12) that were associated specifically with gouty inflammation. All nine sites mapped to active regulatory elements in monocytes. MoLoTool and ReMap analyses indicated that the nine methylation loci overlapped with binding sites of several transcription factors that regulated interleukin-1β production and gouty inflammation. Decreases in PRKCZ and STK11 methylation were also associated with higher numbers of first-degree relatives who also had gout. The gouty-inflammation specific methylome and genome alterations could potentially aid in the identification of novel therapeutic targets.Hepatocellular carcinoma (HCC) is the most common histological type of primary liver cancer and the majority of patients are diagnosed at an advanced stage and have a poor prognosis. AKR1C3 (Aldo-keto reductase family 1 member C3) and AKR1D1 (Aldo-keto reductase family 1 member D1) catalyze the conversion of aldehydes and ketones to alcohols and play crucial roles in multiple cancers. However, the functions of AKR1C3 and AKR1D1 in HCC remain unclear. In our study, data from the public databases were selected as training and validation sets, then 76 HCC patients in our center were chosen as a test set. Bioinformatics methods suggested AKR1C3 was overexpressed in HCC and AKR1D1 was down-regulated. The receiver operating characteristic curve (ROC) analysis was performed and the area under curve (AUC) values of AKR1C3 and AKR1D1 were above 0.7 (0.948, 0.836, respectively). Also, the high expression of AKR1C3 and low expression of AKR1D1 predicted poor prognosis and short median survival time. Then, the knockdown of AKR1C3 and overexpression of AKR1D1 in HCC cells were achieved with lentivirus. And both decreased cell proliferation, restrained cell viability, and inhibited tumorigenesis. Moreover, the gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were conducted and the results showed that AKR1C3 and AKR1D1 might participate in the MAPK/ERK and androgen receptor (AR) signaling pathway. Furthermore, the AR and phosphorylated ERK1/2 were significantly reduced after the suppression of AKR1C3 or overexpression of AKR1D1. Collectively, AKR1C3 and AKR1D1 might serve as candidate diagnostic and prognostic biomarkers for HCC and provide potential targets for HCC treatment.Lumican (LUM), a small leucine-rich proteoglycan, is a component of the extracellular matrix. Abnormal LUM expression is potentially associated with cancer progression. In the present study, we confirmed high LUM mRNA expression in colorectal adenocarcinoma (COAD) through the UALCAN database. The Kaplan-Meier method, univariate, and multivariate COX analysis showed that high LUM expression is an independent determinant of poor prognosis in COAD. A COX regression model was constructed based on clinical information and LUM expression. The receiver operating characteristic (ROC) curve indicated that this model was highly accurate in monitoring COAD prognosis. The co-expression network of LUM was determined by LinkedOmics, which showed that LUM expression was closely related to immune escape and the miR200 family. Furthermore, we studied the co-expression network of LUM and found that LUM could promote tumor metastasis and invasion. The Tumor Immune Estimation Resource website showed that LUM was closely related to immune infiltration and correlated with regulatory T cells, tumour-associated macrophages, and dendritic cells. We found that LUM cultivated cancer progression by targeting the miR200 family to promote epithelial-to-mesenchymal transition. These findings suggest that LUM is a potential target for inhibiting immune escape and carcinogenic pathways.E3 ubiquitin ligase RING finger protein 168 (RNF168) is one of the key proteins in DNA damage repair. Abnormal expression of RNF168 has recently been found in some tumors. However, the role of RNF168 in the development of esophageal squamous cell carcinoma (ESCC) has not been fully elucidated. Here we report that expression of RNF168 in esophageal squamous cell carcinoma is increased with respect to normal esophageal epithelial tissue. Notably, in ESCC patients, increased RNF168 expression was associated with tumor stage and depth of invasion. Knockdown of the RNF168 gene inhibited proliferation of esophageal cancer cells, promoted cell apoptosis, and interfered with cell movement, ultimately inhibiting tumor xenograft growth. Mechanistic studies showed that RNF168 influenced the malignant behavior of esophageal cancer cells by regulating the Wnt/ β-catenin signaling pathway. In addition, RNF168 expression was positively correlated with wingless-type MMTV integration site family member 3A (WNT3A) expression, and high expression of RNF168 and WNT3A predicted a low survival rate. In conclusion, our findings highlight the important role of RNF168 in ESCC tumorigenesis and provide new biomarkers and therapeutic targets for the treatment of ESCC.Ovarian serous carcinoma (OSC), as a common malignant tumor, poses a serious threat to women's health in that epithelial-mesenchymal transformation (EMT)-related modulation becomes heavily implicated in the invasion and progression of OSC. selleck chemicals In this study, two core genes (BUB1B and NDC80) among the 16 hub genes have been identified to be involved in the molecular regulation of EMT and associated with the poor early survival of OSC at stages I+II. Through the Gene Regulatory Networks (GRN) analysis of 15 EMT regulators and core genes, it was revealed that TFAP2A and hsa-miR-655 could elaborately modulate EMT development of OSC. Next genetic variation analysis indicated that EMT regulator ELF3 would also serve as a crucial part in the occurrence and progression of OSC. Eventually, survival investigation suggested that TFAP2A, ELF3 and hsa-miR-655 were significantly associated with the overall survival of progressive OSC patients. Thus, combined with diversified bioinformatic analyses, BUB1B, NDC80, TFAP2A, ELF3 and hsa-miR-655 may act as the key biomarkers for early clinical diagnosis and prognosis evaluation of OSC patients as well as potential therapeutic target-points.

Misdiagnosis, arbitrary charges, annoying queues, and clinic waiting times among others are long-standing phenomena in the medical industry across the world. These factors can contribute to patient anxiety about misdiagnosis by clinicians. However, with the increasing growth in use of big data in biomedical and health care communities, the performance of artificial intelligence (Al) techniques of diagnosis is improving and can help avoid medical practice errors, including under the current circumstance of COVID-19.

This study aims to visualize and measure patients' heterogeneous preferences from various angles of AI diagnosis versus clinicians in the context of the COVID-19 epidemic in China. We also aim to illustrate the different decision-making factors of the latent class of a discrete choice experiment (DCE) and prospects for the application of AI techniques in judgment and management during the pandemic of SARS-CoV-2 and in the future.

A DCE approach was the main analysis method applied in this papbutes are palpable. AI will have a potential market. However, accuracy and diagnosis expenses need to be taken into consideration.

More than 1 in 4 people in the United States aged 65 years and older have type 2 diabetes. For diabetes care, medical nutrition therapy is recommended as a clinically effective intervention. Previous researchers have developed and validated dietary assessment methods using images of food items to improve the accuracy of self-reporting over traditional methods. Nevertheless, little is known about the usability of image-assisted dietary assessment methods for older adults with diabetes.

The aims of this study were (1) to create a food record app for dietary assessments (FRADA) that would support image-assisted dietary assessments, and (2) to evaluate the usability of FRADA for older adults with diabetes.

For the development of FRADA, we identified design principles that address the needs of older adults and implemented three fundamental tasks required for image-assisted dietary assessments capturing, viewing, and transmitting images of food based on the design principles. For the usability assessment of F FRADA, and concerns of older adults with diabetes regarding interactions with FRADA.

This study demonstrates in a lab-based setting not only the usability of FRADA by older adults with diabetes but also potential opportunities using FRADA in real-world settings. The findings suggest implications for creating a smartphone app for an image-assisted dietary assessment. Future work still remains to evaluate the feasibility and validity of FRADA with multiple stakeholders, including older adults with diabetes and dietitians.

This study demonstrates in a lab-based setting not only the usability of FRADA by older adults with diabetes but also potential opportunities using FRADA in real-world settings. The findings suggest implications for creating a smartphone app for an image-assisted dietary assessment. Future work still remains to evaluate the feasibility and validity of FRADA with multiple stakeholders, including older adults with diabetes and dietitians.