Bridging the Gap between TGF-β/Smad Signalling and Tumorigenesis Arising from Clonorchis sinensis Induced Hepatic Fibrosis

Clonorchiasis is a parasitic infection caused by food borne trematode, Clonorchis sinensis that is mainly prevalent in Asian countries, including South Korea, China, northern Vietnam, Japan, as well as far-eastern Russia, in which over 35 million people are the casualties. Clonorchiasis is character...

Full description

Saved in:
Bibliographic Details
Main Authors: Ika Nurzijah, Dina Ratna Juwita
Format: Article
Language:English
Published: Indonesian Society for Cancer Chemoprevention 2018-02-01
Series:ISCC (Indonesian Journal of Cancer Chemoprevention)
Online Access:https://ijcc.chemoprev.org/index.php/ijcc/article/view/201
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1849323197878501376
author Ika Nurzijah
Dina Ratna Juwita
author_facet Ika Nurzijah
Dina Ratna Juwita
author_sort Ika Nurzijah
collection DOAJ
description Clonorchiasis is a parasitic infection caused by food borne trematode, Clonorchis sinensis that is mainly prevalent in Asian countries, including South Korea, China, northern Vietnam, Japan, as well as far-eastern Russia, in which over 35 million people are the casualties. Clonorchiasis is characterized by the development of hepatic fibrosis. Upon chronic liver injury following the C. sinensis infection, hepatic fibrosis develops into cholangiocarcinoma with a concomitant genetic and epigenetic mutations. Cholangiocarcinoma represents important clinical manifestation of C. sinensis infection and causes high rate of morbidity. TGF- β/Smad signalling is known to initiate hepatic fibrosis following the hepatic injury. However, little is known about the role of TGF- β/Smad signalling during C. sinensis induced hepatic injury and the underlying contribution of TGF- β/Smad signalling in the development of cholangicarcinoma. The expression dynamic of TGF-β/Smad signalling and their role in the development of hepatic fibrosis in C. sinensis infected BALB/c mice have been investigated. Concomitantly but irrespective to C. sinensis infection, the role of hepatic epithelial TGF-β during hepatic fibrosis and the development of cholangiocarcinoma arising from hepatic epithelial cells have also been dissected. Both findings will be reviewed in this paper. Thereby, the link between TGF-β/Smad signalling, hepatic fibrosis during C sinensis infection, and cholangiocarcinoma could be drawn clearly. Keywords: Clonorchis sinensis, TGF-β/Smad signalling, Hepatic fibrosis, Cholangiocarcinoma
format Article
id doaj-art-e2b652bd0a5b4249b32fba2ff36f682b
institution Kabale University
issn 2088-0197
2355-8989
language English
publishDate 2018-02-01
publisher Indonesian Society for Cancer Chemoprevention
record_format Article
series ISCC (Indonesian Journal of Cancer Chemoprevention)
spelling doaj-art-e2b652bd0a5b4249b32fba2ff36f682b2025-08-20T03:49:07ZengIndonesian Society for Cancer ChemopreventionISCC (Indonesian Journal of Cancer Chemoprevention)2088-01972355-89892018-02-0191414610.14499/indonesianjcanchemoprev9iss1pp41-46156Bridging the Gap between TGF-β/Smad Signalling and Tumorigenesis Arising from Clonorchis sinensis Induced Hepatic FibrosisIka Nurzijah0Dina Ratna Juwita1University of Muhammadiyah PurwokertoUniversity of Muhammadiyah PurwokertoClonorchiasis is a parasitic infection caused by food borne trematode, Clonorchis sinensis that is mainly prevalent in Asian countries, including South Korea, China, northern Vietnam, Japan, as well as far-eastern Russia, in which over 35 million people are the casualties. Clonorchiasis is characterized by the development of hepatic fibrosis. Upon chronic liver injury following the C. sinensis infection, hepatic fibrosis develops into cholangiocarcinoma with a concomitant genetic and epigenetic mutations. Cholangiocarcinoma represents important clinical manifestation of C. sinensis infection and causes high rate of morbidity. TGF- β/Smad signalling is known to initiate hepatic fibrosis following the hepatic injury. However, little is known about the role of TGF- β/Smad signalling during C. sinensis induced hepatic injury and the underlying contribution of TGF- β/Smad signalling in the development of cholangicarcinoma. The expression dynamic of TGF-β/Smad signalling and their role in the development of hepatic fibrosis in C. sinensis infected BALB/c mice have been investigated. Concomitantly but irrespective to C. sinensis infection, the role of hepatic epithelial TGF-β during hepatic fibrosis and the development of cholangiocarcinoma arising from hepatic epithelial cells have also been dissected. Both findings will be reviewed in this paper. Thereby, the link between TGF-β/Smad signalling, hepatic fibrosis during C sinensis infection, and cholangiocarcinoma could be drawn clearly. Keywords: Clonorchis sinensis, TGF-β/Smad signalling, Hepatic fibrosis, Cholangiocarcinomahttps://ijcc.chemoprev.org/index.php/ijcc/article/view/201
spellingShingle Ika Nurzijah
Dina Ratna Juwita
Bridging the Gap between TGF-β/Smad Signalling and Tumorigenesis Arising from Clonorchis sinensis Induced Hepatic Fibrosis
ISCC (Indonesian Journal of Cancer Chemoprevention)
title Bridging the Gap between TGF-β/Smad Signalling and Tumorigenesis Arising from Clonorchis sinensis Induced Hepatic Fibrosis
title_full Bridging the Gap between TGF-β/Smad Signalling and Tumorigenesis Arising from Clonorchis sinensis Induced Hepatic Fibrosis
title_fullStr Bridging the Gap between TGF-β/Smad Signalling and Tumorigenesis Arising from Clonorchis sinensis Induced Hepatic Fibrosis
title_full_unstemmed Bridging the Gap between TGF-β/Smad Signalling and Tumorigenesis Arising from Clonorchis sinensis Induced Hepatic Fibrosis
title_short Bridging the Gap between TGF-β/Smad Signalling and Tumorigenesis Arising from Clonorchis sinensis Induced Hepatic Fibrosis
title_sort bridging the gap between tgf β smad signalling and tumorigenesis arising from clonorchis sinensis induced hepatic fibrosis
url https://ijcc.chemoprev.org/index.php/ijcc/article/view/201
work_keys_str_mv AT ikanurzijah bridgingthegapbetweentgfbsmadsignallingandtumorigenesisarisingfromclonorchissinensisinducedhepaticfibrosis
AT dinaratnajuwita bridgingthegapbetweentgfbsmadsignallingandtumorigenesisarisingfromclonorchissinensisinducedhepaticfibrosis