Page 157 - ebook HCC

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PROGRAMME AND ABSTRACTSAND ABSTRACTS
GENEV
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154 PROGRAMME GENEVA, SWITZERLANDA, SWITZERLAND EASL HCC SUMMITHCC SUMMIT 155
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FEBRUAR
FEBRUARY 13 - 16, 2014Y 13 - 16, 2014
Poster Board Number B43 Poster Board Number B44
MICRORNA-125B MODULATES CELL GROWTH, ANALYSIS OF DLC 1 GENE POLYMORPHISM
METABOLISM AND HBV REPLICATION VIA AMONG HEPATOCELLULAR CARCINOMA
LIN28B/LET7 AXIS PATIENTS IN INDIA

Wanyu Deng 1 Balachandar Vellingiri , Mohana Devi Subramaniam , Meyyazhagan Arun ,
2
1
2
1 Institute of Virology, Essen, Germany Balasubramanian Balamuralikrishnan , Keshavarao Sasikala 2
2
1 Human Molecular Genetics Laboratory, Department of Zoology, Bharathiar University,
Corresponding author’s e-mail: wanyu0330@126.com Coimbatore , Zoology, Human Molecular Genetics Laboratory, Department of Zoology,
2
Bharathiar University, Coimbatore - 641 046, Tamil Nadu, India, Coimbatore, India
Introduction: Previously, we showed that miR-1 upregulated HBV replication through Corresponding author’s e-mail: geneticbala@yahoo.co.in
enhancement of HBV core promotor activity and it also inhibited cell growth. However,
miR-1 was expressed at a low level in hepatocytes.
Introduction: Hepatocellular carcinoma (HCC) is the fifth most frequent malignant tumour
Aims: Here, we asked whether miRNAs highly expressed in hepatocytes could also in man and the third for cancer related mortality worldwide, especially in parts of Asia
modulate HBV replication. and Africa. The development of HCC is found to have both environmental and genetic
mechanism. The environmental aspects comprises chronic infection with hepatitis B
Methodology: A number of miRNAs with decreased expression in hepatocellular (HBV) and C virus (HCV), intake of alcohol, smoking, aflatoxin exposure, cirrhosis and
carcinoma were tested for their ability to influence HBV replication at different levels male gender. Loss of gene deleted in liver cancer 1 (DLC1) gene has been associated in
BASIC POSTER ABSTRACTS control of cell proliferation was examined by transfection in established hepatoma cell Aims: The aim of the present study was to analyze the relationship between DLC1 gene BASIC POSTER ABSTRACTS
the progression of HCC.
including viral transcription, assembly, and virion production. Their involvement in the
lines. RNA sequence assay was explored to determine the global gene expression pattern
polymorphism and risk of HCC among South Indian population.
in cells transfected with miRNAs.
Results: Among the tested miRNAs, miR-125b was found enhance HBV replication
Genotyping of T>G, G>A, and C>T for HCC patients and controls was performed by
significantly. In constrast to miR-1, miR-125b did not regulate HBV transcription but
increased HBV replicative intermediate and nucleocapsid formation. It exerted a Methodology: Blood samples from 98 HCC patients and 98 controls were collected.
polymerase chain reaction- based restriction fragment length polymorphism (PCR-RFLP).
synergistic effect on upregulation of HBV replication with miR-1. MiR-125b down regulated The association among HCC and polymorphism were analyzed.
RB phosphorylation and inhibited hepatoma cells proliferation by blocking cell cycle at
the G1/S phase transition. Moreover, miR-125b could modulate a number of liver-specific Results: The study on DLC1 polymorphism demonstrated differences in allele frequencies
metabolic pathways. MiR-125b reduced LIN28B and thereby upregulated the let-7 family compared to controls. Among three genotypes C/C genotype has a higher susceptibility to
members to enhance HBV replication. HCC among the study population.

Conclusions: This is the first time we identified a specific factor that positively influence Conclusions: The genetic variants analyzed may lead to inter individual susceptibility
HBV replication in the post-transcriptional process. Our results demonstrated that some to HCC and very limited role of genetic polymorphism has been investigated and the
miRNAs with the ability to arrest the cell cycle at the G1 phase may preferentially up- combined effect of these variants may interact by boosting up the risk of HCC in the study
regulate HBV replication. We also found miR-125b could regulate lin28b/let7 axis. population.