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

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

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

OBJECTIVETo evaluate the mRNA and protein expressions of peroxiredoxin II (PrxII) in hepatocellular carcinoma (HCC) and their significance.

METHODSHCC was induced by aflatoxin B1 (AFB1) in 6 tree shrews (Tupaia belangeri chinensis). The expression levels of PrxII mRNA and protein were detected by reverse transcriptase polymerase chain reaction (RT-PCR) and Western blot on HCC tissues and on their surrounding liver tissues (para-HCC). Biopsied liver tissues were taken before the HCC induction (pre-HCC) from the same animals and from a group of blank controlled animals that served as controls. Liver biopsy specimens from 18 cases of human HCC and from 17 healthy human volunteers were studied using the same methods.

RESULTSThe mRNA and protein expressions of PrxII in tree shrew HCC tissues were significantly higher than those in para-HCC and pre-HCC tissues, and also higher than those in the liver tissues from the control animals (all P < 0.05). The expression levels of PrxII mRNA and protein in human HCC tissues were also significantly higher than those in their para-HCC tissues and in the human normal liver tissues (P < 0.05).

CONCLUSIONPrxII might play an important role in hepatocarcinogenesis and might be used as a molecular target for HCC prevention and treatment.

Adult ; Aged ; Animals ; Carcinoma, Hepatocellular ; metabolism ; pathology ; Female ; Humans ; Liver ; metabolism ; pathology ; Liver Neoplasms ; metabolism ; pathology ; Liver Neoplasms, Experimental ; metabolism ; pathology ; Male ; Middle Aged ; Peroxiredoxins ; genetics ; Tupaiidae

Antigens, CD ; genetics ; metabolism ; Carcinoma, Hepatocellular ; metabolism ; pathology ; Humans ; Liver Neoplasms ; metabolism ; pathology ; Tetraspanin 24

Carcinoma, Hepatocellular ; metabolism ; pathology ; Core Binding Factor Alpha 3 Subunit ; metabolism ; Female ; Hepatocytes ; metabolism ; Humans ; Liver ; metabolism ; pathology ; Liver Neoplasms ; metabolism ; pathology ; Male ; RNA, Messenger ; genetics

Adult ; Carcinoma, Hepatocellular ; metabolism ; pathology ; Humans ; Liver ; pathology ; Liver Neoplasms ; metabolism ; pathology ; Middle Aged ; RNA, Messenger ; genetics ; Tumor Suppressor Proteins ; genetics ; metabolism

This study explored the double lethal effects of pEGFP-C1-wtp53/junB fusion gene on hepatocellular carcinoma (HCC) cells. wtp53/junB fusion gene was constructed and transformed into HepG2 cell line. Expression of KAI1 was detected by quantitative real-time PCR and Western blotting, cells apoptosis rate was detected by flow cytometry, proliferation of cells was detected byMTT chromometry, cell transmigration was detected by using transwell systems. The results showed that after transformation with pEGFP-C1-wtp53/JunB, the expression level of KAI1 protein was up-regulated, being 8.13 times the blank control group in HepG2 cells and significantly higher than 2.87 times which transformed with pEGFP-C1-JunB, 3.11 times which transformed with pEGFP-C1-wtp53 (P<0.001). Apoptosis rate of HepG2 cells transformed with pEGFP-C1-wtp53/JunB was significantly higher than that of other groups (P<0.001), and invasive ability of HepG2 cells transformed with pEGFP-C1-wtp53/JunB was significantly lower than other groups(P<0.001). It was concluded that the fusion gene of wtp53 and JunB could not only inhibit the growth of hepatoma cells and promote tumor cell apoptosis, but also suppress the invasive ability of tumor cells by up-regulating the expression of KAI1.
Carcinoma, Hepatocellular ; genetics ; metabolism ; pathology ; Cell Line, Tumor ; Hep G2 Cells ; Humans ; Liver Neoplasms ; genetics ; metabolism ; pathology ; Transcription Factors ; genetics ; metabolism ; Tumor Suppressor Protein p53 ; genetics ; metabolism

Case-Control Studies ; Gene Expression ; Humans ; Liver ; metabolism ; pathology ; Liver Neoplasms ; metabolism ; pathology ; Protein-Serine-Threonine Kinases ; genetics ; metabolism ; Proto-Oncogene Proteins ; genetics ; metabolism