LINC00667: A Novel Vital Oncogenic LincRNA.

Long intergenic noncoding RNAs (lincRNAs) have a variety of properties that differ from those of messenger RNAs (mRNAs) encoding proteins. Long intergenic nonprotein coding RNA 667 (LINC00667) is a non-coding transcript located on chromosome 18p11.31. Recently, many studies have found that LINC00667 can enhance the progression of various cancers and play a key part in a lot of diseases, such as tumorigenesis. Therefore, LINC00667 can be recognized as a potential biomarker and therapeutic target. So, we reviewed the biological functions, relevant mechanisms, as well as clinical significance of LINC00667 in several human cancers in detail.

LncRNA KCNQ1OT1: Molecular mechanisms and pathogenic roles in human diseases.

Long non-coding RNAs (lncRNAs) exhibit a length more than 200 nucleotides and they are characterized by non-coding RNAs (ncRNA) not encoded into proteins. Over the past few years, the role and development of lncRNAs have aroused the rising attention of researchers. To be specific, KCNQ1OT1, the KCNQ1 opposite strand/antisense transcript 1, is clearly classified as a regulatory ncRNA. KCNQ1OT1 is capable of interacting with miRNAs, RNAs and proteins, thereby affecting gene expression and various cell functions (e.g., cell proliferation, migration, epithelial-mesenchymal transition (EMT), apoptosis, viability, autophagy and inflammation). KCNQ1OT1 is dysregulated in a wide range of human diseases (e.g., cardiovascular disease, cancer, diabetes, osteoarthritis, osteoporosis and cataract), and it is speculated to act as a therapeutic target for treating various human diseases. On the whole, this review aims to explore the biological functions, underlying mechanisms and pathogenic roles of KCNQ1OT1 in human diseases.

NEAT1: A Novel Long Non-coding RNA Involved in Mediating Type 2 Diabetes and its Various Complications.

BACKGROUND: Nuclear-enriched abundant transcript 1 (abbreviated as NEAT1) is a long-chain noncoding RNA involved in various physiological and pathological processes. This study aimed to clarify the effect and molecule system of NEAT1 within non-alcoholic fatty liver disease (NAFLD) as well as type 2 diabetes (T2DM). METHODS: In this review, current studies concerning mechanisms of NEAT1l, in the development of type 2 diabetes and its complications have been summarized and analyzed. Also, we searched the papers based on NEAT1 related to NAFLD. The related studies were obtained through a systematic search of Pubmed. RESULTS: NEAT1 displays a close correlation with how T2DM occurs and develops, and it was confirmed to be significantly up-regulated in T2DM and its various complications (e.g., diabetics nephropathy, diabetics cardiomyopathy, diabetics retinopathy as well as diabetic neuropathy). Besides, NEAT1 is capable of impacting the occurrence, development and prognosis of NAFLD and T2DM. CONCLUSION: LncRNA NEAT1 is likely to act as a novel therapeutic target for T2DM and its complications. Moreover, non-alcoholic fatty liver disease is also correlated with NEAT1.

The Role of LncRNA TUG1 in Obesity-related Diseases.

As the living standards of people are increasingly improved, obesity has become a hotspot in our daily life. Obesity has been found as a chronic and recurrent disease with serious adverse consequences. Over the past few years, several articles indicated that long non-coding RNA taurine increased gene 1 (lncRNA TUG1), a useful RNA, which was indicated to show a relationship to obesity- related disease occurrence and development. Exosomes are recognized as an emerging research field that includes substances actively involved in regulating the molecular mechanisms of disease. This review summarizes the current relevant TUG1 in different molecular pathways of obesityassociated diseases, the correlation between exosomes and TUG1, or obesity-associated diseases. The aim is to explore TUG1 as a novel target for obesity, which can deepen the knowledge regarding the epigenetic regulation pathway. Furthermore, it is expected to focus on diseases associated with obesity treatment and diagnosis.

Long Non-Coding RNA GAS5 in Age-Related Diseases.

Aging refers to a natural process and a universal phenomenon in all cells, tissues, organs, and the whole organism. Long non-coding RNAs (lncRNAs) are non-coding RNAs with a length of 200 nucleotides. LncRNA growth arrest-specific 5 (lncRNA GAS5) is often down-regulated in cancer. The accumulation of lncRNA GAS5 has been found to be able to inhibit cancer growth, invasion, and metastasis while enhancing the sensitivity of cells to chemotherapy drugs. LncRNA GAS5 can be a signaling protein, which is specifically transcribed under different triggering conditions. Subsequently, it is involved in signal transmission in numerous pathways as a signal node. LncRNA GAS5, with a close relationship to multiple miRNAs, was suggested to be involved in the signaling pathway under three action modes (i.e., signal, bait, and guidance). LncRNA GAS5 was found to be involved in different age-related diseases (e.g., rheumatoid arthritis, type 2 diabetes, atherosclerosis, osteoarthritis, osteoporosis, multiple sclerosis, cancer, etc.). This study mainly summarized the regulatory effect exerted by lncRNA GAS5 on age-related diseases.

H19: A Vital Long Noncoding RNA in the Treatment of Diabetes and Diabetic Complications.

BACKGROUND: Increasing academic efforts have been made to explore the correlation of long noncoding RNAs (lncRNAs) with human diseases, particularly metabolic diseases like diabetes mellitus. Taking lncRNA H19 as an example, this review intends to reveal the functions and mechanism of lncRNA H19 in diabetes mellitus and diabetic complications. METHODS: The research results associated with lncRNA H19 and diabetes mellitus are collected and summarized on PubMed. CONCLUSION: LncRNA H19 is a potential instructive marker for the treatment of diabetes mellitus and diabetic complications.

Dietary Intake of Hydrolyzable Tannins and Condensed Tannins to Regulate Lipid Metabolism.

Lipid metabolism disorder is a multifactor issue, which contributes to several serious health consequences, such as obesity, hyperlipidemia, atherosclerosis diabetes, non-alcoholic fatty liver, etc. Tannins, applied as naturally derived plants, are commonly used in the study of lipid metabolism disease with excellent safety and effectiveness while producing less toxic and side effects. Meanwhile, recognition of the significance of dietary tannins in lipid metabolism disease prevention has increased. As suggested by existing evidence, dietary tannins can reduce lipid accumulation, block adipocyte differentiation, enhance antioxidant capacity, increase the content of short-chain fatty acids, and lower blood lipid levels, thus alleviating lipid metabolism disorder. This study is purposed to sum up and analyze plenty of documents on tannins, so as to provide the information required to assess the lipid metabolism of tannins.

Astragaloside IV ameliorates fat metabolism in the liver of ageing mice through targeting mitochondrial activity.

Astragaloside IV (AST) is a major bioactive compound of Radix Astragali with medical and health benefits. Previous studies have found that AST can reduce the body weights of high-fat diet fed mice. However, the effect of AST on fat metabolism of ageing mice is unclear. In this study, naturally ageing mice were administered intragastrically with AST at 30 mg/kg/day (ageing + AST-L group) and 90 mg/kg/day (ageing + AST-H group) for 16-20 months. Adult (4 months old) and ageing mice were given 1% sodium carboxyl methylcellulose as vehicle. Energy metabolism-related biological parameters of living mice were examined. Moreover, mRNA and protein levels of key enzymes/proteins involved in triglyceride (TG) lipolysis, fatty acid ß-oxidation (FAO), ketone body (KB) production and mitochondrial respiratory chain were also examined after sacrifice. Results demonstrated that treatment with AST significantly reduced body weight, white fat and liver/body weight ratio of ageing mice, significantly reduced serum/hepatic TG levels, respiratory quotient, promoted fatty acid mobilization in white adipose tissue, mitochondrial FAO and KB production and mitochondrial biosynthesis/functions in the liver of ageing mice. AST also up-regulated the expression of phosphorylated AMP-activated protein kinase, acetyl-CoA carboxylase, acetyl-coenzyme A synthetase, carnitine palmitoyltransferase 1a/1b, enoyl coenzyme A hydratase-short chain, acyl-CoA dehydrogenase medium chain and mitochondrial 3-hydroxy-3-methylglutaryl-CoA synthase-2 involved in fat metabolism. These results indicated that mitochondrial activity could be the target of AST to treat abnormal fat metabolism during ageing.