With the improvement of high-throughput genomic technology such as microarray and next-generation sequencing over the last ten to twenty year, we have come to know that the portion of the genome responsible for protein coding constitutes just approximately 1.5%. The remaining 98.5% of the genome not responsible for protein coding have been regarded as 'junk DNA'. More recently, however, 'Encyclopedia of DNA elements project' revealed that most of the junk DNA were transcribed to RNA regardless of being translated into proteins. In addition, many reports support that a lot of these non-coding RNAs play a role in gene regulation. In fact, there are various functioning short non-coding RNAs including rRNA, tRNA, small interfering RNA, and micro RNA. Mechanisms of these RNAs are relatively well-known. Until recently, however, little is known about long non-coding RNAs which consist of 200 nucleotides or more. In this article, we will review the representative long non-coding RNAs which have been reported to be related to gastrointestinal cancers and to play a certain role in its pathogenesis.
Gastrointestinal Neoplasms/*genetics/*metabolism/pathology ; Humans ; Liver Neoplasms/genetics/metabolism/pathology ; RNA, Long Noncoding/genetics/*metabolism

With the improvement of high-throughput genomic technology such as microarray and next-generation sequencing over the last ten to twenty year, we have come to know that the portion of the genome responsible for protein coding constitutes just approximately 1.5%. The remaining 98.5% of the genome not responsible for protein coding have been regarded as 'junk DNA'. More recently, however, 'Encyclopedia of DNA elements project' revealed that most of the junk DNA were transcribed to RNA regardless of being translated into proteins. In addition, many reports support that a lot of these non-coding RNAs play a role in gene regulation. In fact, there are various functioning short non-coding RNAs including rRNA, tRNA, small interfering RNA, and micro RNA. Mechanisms of these RNAs are relatively well-known. Until recently, however, little is known about long non-coding RNAs which consist of 200 nucleotides or more. In this article, we will review the representative long non-coding RNAs which have been reported to be related to gastrointestinal cancers and to play a certain role in its pathogenesis.
Gastrointestinal Neoplasms/*genetics/*metabolism/pathology ; Humans ; Liver Neoplasms/genetics/metabolism/pathology ; RNA, Long Noncoding/genetics/*metabolism

Objective: Cluster classification based on m6A methylation regulators and construct prognostic evaluation model. Methods: Utilizing consensus cluster to classify the liver cancer samples form TCGA based on the expression of 13 m6A methylation regulators, and verify the function and prognostic significance of the clustered subtypes. Marker genes were further screened to construct a risk prediction model for evaluating the prognosis of liver cancer patients. Results: The two clustered subtypes based on m6A methylation regulators showed significant differences in the prognosis value of liver cancer patients (P=0.048), and 38 prognostic markers related to m6A methylation in liver cancer were screened from the subgroup with poor prognosis. Two m6A regulatory genes, YTHDF1 and YTHDF2, are proved with adverse prognosis by univariate cox analysis (P<0.05, Hazard ratio>1). We used Lasso regression method to build risk assessment model and effectively predicted the prognosis status of liver cancer patients within 4 years (4-year AUC=0.685, 3-year AUC=0.669). Moreover, the assessment model was validated in another dataset of Asia liver cancer patients. Conclusion: The study provided ideas for studying m6A methylation in liver cancer, and the risk prediction model can be used to evaluate the short-term prognosis of liver cancer patients.
Humans ; Methylation ; Prognosis ; Adenosine/metabolism* ; Liver Neoplasms/genetics* ; RNA/genetics*

Carcinoma, Hepatocellular ; metabolism ; Glycoproteins ; biosynthesis ; genetics ; Humans ; Hyaluronan Receptors ; biosynthesis ; genetics ; Liver ; metabolism ; Liver Neoplasms ; metabolism ; Osteopontin ; biosynthesis ; genetics

Carcinoma, Hepatocellular ; metabolism ; pathology ; DNA-Binding Proteins ; genetics ; metabolism ; Humans ; Liver Neoplasms ; metabolism ; pathology ; Phosphoproteins ; genetics ; metabolism ; RNA, Messenger ; genetics

OBJECTIVETo investigate the expression of integrin beta 1 in hepatic cirrhosis (HC) and hepatocellular carcinoma (HCC).

METHODSThe expression of integrin beta 1 in HCC, HC and normal liver tissues was detected by reverse transcriptase-polymerase chain reaction (RT-PCR) and laser scanning confocal microscopy (LSCM). The association between the integrin beta 1 expression and clinical pathological features were analyzed.

RESULTS(1) The levels of integrin beta 1 mRNA and protein in the HCC (1.30+/-0.24, 90.50+/-33.50) and HC (1.58+/-0.31, 123.10+/-38.90) were much higher than that in the normal hepatic tissue (0.37+/-0.08, 11.90+/-6.00) (P less than 0.05). (2) The expression of integrin beta 1 was associated with HC (r = 0.692), Edmondson pathologic grade (F = 13.618), encapsulation (F = 17.857) and metastasis (F = 38.857) (P less than 0.01).

CONCLUSIONSIntegrin beta 1 may play an important role in the development of hepatic fibrosis, hepatic cirrhosis and hepatocellular carcinoma.

Carcinoma, Hepatocellular ; metabolism ; pathology ; Humans ; Integrin beta1 ; genetics ; metabolism ; Liver ; metabolism ; Liver Cirrhosis ; metabolism ; pathology ; Liver Neoplasms ; metabolism ; pathology ; RNA, Messenger ; genetics

Animals ; CD40 Ligand ; genetics ; metabolism ; Carcinoma, Hepatocellular ; genetics ; metabolism ; therapy ; Genetic Therapy ; Liver Neoplasms ; genetics ; metabolism ; therapy ; Mice ; Neoplasms, Multiple Primary ; genetics ; metabolism ; therapy ; Transgenes ; genetics

Carcinoma, Hepatocellular ; metabolism ; Glypicans ; biosynthesis ; genetics ; Humans ; Liver Neoplasms ; metabolism ; RNA, Messenger ; biosynthesis ; genetics

Carcinoma, Hepatocellular ; genetics ; metabolism ; Humans ; Liver Neoplasms ; genetics ; metabolism ; Signal Transduction

Lipid metabolism is a complex physiological process, which is closely related to nutrient regulation, hormone balance and endocrine function. It involves the interactions of multiple factors and signal transduction pathways. Lipid metabolism disorder is one of the main mechanisms to induce a variety of diseases, such as obesity, diabetes, non-alcoholic fatty liver disease, hepatitis, hepatocellular carcinoma and their complications. At present, more and more studies have found that the "dynamic modification" of N⁶-adenylate methylation (m⁶A) on RNA represents a new "post-transcriptional" regulation mode. m⁶A methylation modification can occur in mRNA, tRNA, ncRNA, etc. Its abnormal modification can regulate gene expression changes and alternative splicing events. Many latest references have reported that m⁶A RNA modification is involved in the epigenetic regulation of lipid metabolism disorder. Based on the major diseases induced by lipid metabolism disorders, we reviewed the regulatory roles of m⁶A modification in the occurrence and development of those diseases. These overall findings inform further in-depth investigations of the underlying molecular mechanisms regarding the pathogenesis of lipid metabolism disorders from the perspective of epigenetics, and provide reference for health prevention, molecular diagnosis and treatment of related diseases.
Humans ; Methylation ; Epigenesis, Genetic ; Lipid Metabolism/genetics* ; Lipid Metabolism Disorders/genetics* ; Liver Neoplasms ; RNA