scholarly journals Quantification of Pregenomic RNA and Covalently Closed Circular DNA in Hepatitis B Virus-Related Hepatocellular Carcinoma

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
Fugui Bai ◽  
Yoshihiko Yano ◽  
Takumi Fukumoto ◽  
Atsushi Takebe ◽  
Motofumi Tanaka ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Circular Dna ◽  
Expression Levels ◽  
Covalently Closed Circular Dna ◽  
Occult Hbv ◽  
Significant Difference ◽  
B Virus ◽  
Liver Tissues

Pregenomic RNA (pgRNA) is generated from covalently closed circular DNA (cccDNA) and plays important roles in viral genome amplification and replication. Hepatic pgRNA and cccDNA expression levels indicate viral persistence and replication activity. This study was aimed to measure hepatic pgRNA and cccDNA expression levels in various states of hepatitis B virus (HBV) infection. Thirty-eight hepatocellular carcinoma (HCC) patients, including 14 positive for hepatitis B surface antigen (HBsAg) and 24 negative for HBsAg but positive for anti-hepatitis B core (anti-HBc) antibody, were enrolled in this study. In HBsAg-negative but anti-HBc-positive group, HBV-DNA was detected in 20 of 24 (83%) noncancerous liver tissues for at least two genomic regions based on polymerase chain reaction (PCR) analysis. pgRNA and cccDNA expression levels in occult HBV-infected patients were significantly lower than those in HBsAg-positive patients (P<0.001). pgRNA and cccDNA in cancerous tissues were also detected without significant difference from those in noncancerous tissues. In conclusion, cccDNA and pgRNA are detected and represented HBV replication not only in noncancerous but also in cancerous liver tissues. In addition, the replication is shown in not only patients with HBsAg-positive but also occult HBV-infected patients, suggesting the contribution to HCC development.

Quantification of hepatitis B virus covalently closed circular DNA in patients with hepatocellular carcinoma

2006 ◽  
Vol 45 (4) ◽  
pp. 553-559 ◽  
Author(s):  
Danny Ka-Ho Wong ◽  
Man-Fung Yuen ◽  
Ronnie Tung-Ping Poon ◽  
John Chi-Hang Yuen ◽  
James Fung ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Circular Dna ◽  
Covalently Closed Circular Dna ◽  
B Virus

scholarly journals LncRNA XIST upregulates TRIM25 via negatively regulating miR-192 in hepatitis B virus-related hepatocellular carcinoma

2021 ◽  
Vol 27 (1) ◽  
Author(s):  
Jiancheng Wang ◽  
Gang Yin ◽  
Hu Bian ◽  
Jiangli Yang ◽  
Pengcheng Zhou ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Expression Levels ◽  
Qrt Pcr ◽  
B Virus ◽  
Lncrna Xist ◽  
Direct Target ◽  
And Migration ◽  
Proliferation And Migration

Abstract Background Long non-coding RNA (lncRNA) XIST has been implicated in the progression of a variety of tumor diseases. The purpose of this study was to explore the molecular role of lncRNA XIST in human hepatitis B virus (HBV)-related hepatocellular carcinoma (HCC). Methods The expression levels of lncRNA XIST, miR-192 and TRIM25 in HBV-related HCC tissues and HepG2.2.15 cells were detected by qRT-PCR. Biological information and luciferin gene reporter assay were performed to detect the interaction among lncRNA XIST, miR-192 and TRIM25. CCk-8 assay, wound healing assay and colony formation assay were conducted to detect the proliferation and migration ability of HepG2.2.15 cells. Results qRT-PCR results showed that the expression levels of lncRNA XIST were remarkably increased in HBV-related HCC tissues and HepG2.2.15 cells. In addition, miR-192 was a direct target gene of lncRNA XIST, and the expression of miR-192 and lncRNA XIST were negatively correlated. Moreover, overexpression of miR-192 observably inhibited the proliferation and migration of HCC cells, while overexpression of lncRNA XIST showed an opposite effect. Furthermore, TRIM25 was a direct target of miR-192, and lncRNA XIST could up-regulate the expression of TRIM25 by targeting miR-192. Conclusion LncRNA XIST could up-regulate the expression of TRIM25 by targeting and binding to miR-192, thus accelerating the occurrence and development of HCC.

The association between hepatitis B virus mutations and the risk of liver disease and hepatocellular carcinoma

2021 ◽  
Vol 21 ◽  
Author(s):  
Hassan Akrami ◽  
Mohammad Rafiee Monjezi ◽  
Shahrzad Ilbeigi ◽  
Farshid Amiri ◽  
Mohammad Reza Fattahi
Keyword(s):  
Hepatocellular Carcinoma ◽  
Liver Disease ◽  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Immune Escape ◽  
Vaccine Failure ◽  
Occult Hbv Infection ◽  
Occult Hbv ◽  
B Virus ◽  
The World

: Hepatitis B virus [HBV], the best-described hepadnavirus, distributed all around the world and may lead to chronic and acute liver disease, cirrhosis, and hepatocellular carcinoma. Despite the advancement in treatment against HBV, an error-prone reverse transcriptase which is require for HBV replication as well as host immune pressure lead to constant evolution and emergence of genotypes, sub-genotypes and mutant viruses; so, HBV will be remained as a major healthcare problem around the world. This review article mainly focuses on the HBV mutations which correlated to occult HBV infection, Immune scape, vaccine failure and eventually liver cirrhosis and HCC. Current study indicated that preS/S region mutations are related to vaccine failure, immune escape, occult HBV infection and the occurrence of HCC. Whereas, P region Mutations may lead to drug resistance to NA antivirals. PreC/C region mutations are associated to HBeAg negativity, immune escape, and persistent hepatitis. Moreover, X region Mutations play an important role in HCC development.

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