HULC: an oncogenic long non‐coding RNA in human cancer

Highly up‐regulated in liver cancer (HULC) was originally identified as the most overexpressed long non‐coding RNA in hepatocellular carcinoma. Since its discovery, the aberrant up‐regulation of HULC has been demonstrated in other cancer types, including gastric cancer, pancreatic cancer, osteosarco...

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Vydáno v:Journal of cellular and molecular medicine Ročník 21; číslo 2; s. 410 - 417
Hlavní autoři: Yu, Xin, Zheng, Heyi, Chan, Matthew T.V., Wu, William Ka Kei
Médium: Journal Article
Jazyk:angličtina
Vydáno: England John Wiley & Sons, Inc 01.02.2017
John Wiley and Sons Inc
Témata:
Angiogenesis
Biomarkers
Bone cancer
cancer
Carcinogenesis - genetics
Cell growth
Cholesterol
Colorectal cancer
Colorectal carcinoma
Drug development
Esophageal cancer
Esophagus
Gastric cancer
Gene expression
Gene Expression Regulation, Neoplastic
Genetic diversity
Hepatitis
Hepatitis B
Hepatitis B virus - physiology
Hepatocellular carcinoma
HULC
Humans
Hyperplasia
Kinases
Lipid metabolism
Liver cancer
long non‐coding RNAs
Lymphatic system
Metastases
Metastasis
Models, Biological
Molecular modelling
Neoplasms - genetics
Non-coding RNA
oncogene
Osteosarcoma
Pancreatic cancer
prognosis
Proteins
Review
Ribonucleic acid
RNA
RNA, Long Noncoding - genetics
RNA, Long Noncoding - metabolism
Sarcoma
Sphingosine kinase
Stem cells
Studies
Transcription factors
Tumorigenesis
Tumors
cancer
long non-coding RNAs
oncogene
prognosis
HULC
ISSN:1582-1838, 1582-4934, 1582-4934
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Abstract Highly up‐regulated in liver cancer (HULC) was originally identified as the most overexpressed long non‐coding RNA in hepatocellular carcinoma. Since its discovery, the aberrant up‐regulation of HULC has been demonstrated in other cancer types, including gastric cancer, pancreatic cancer, osteosarcoma and hepatic metastasis of colorectal cancer. Recent discoveries have also shed new light on the upstream molecular mechanisms underlying HULC deregulation. As an oncogene, HULC promotes tumorigenesis by regulating multiple pathways, such as down‐regulation of EEF1E1, promotion of abnormal lipid metabolism, and up‐regulation of sphingosine kinase 1. Pertinent to clinical practice, a genetic variant in the HULC gene has been found to alter the risk for hepatocellular carcinoma and oesophageal cancer, whereas cancer patients with high or low expression of HULC exhibit different clinical outcome. These findings highlighted the pathogenic role and clinical utility of HULC in human cancers. Further efforts are warranted to promote the development of HULC‐directed therapeutics.
AbstractList Highly up‐regulated in liver cancer (HULC) was originally identified as the most overexpressed long non‐coding RNA in hepatocellular carcinoma. Since its discovery, the aberrant up‐regulation of HULC has been demonstrated in other cancer types, including gastric cancer, pancreatic cancer, osteosarcoma and hepatic metastasis of colorectal cancer. Recent discoveries have also shed new light on the upstream molecular mechanisms underlying HULC deregulation. As an oncogene, HULC promotes tumorigenesis by regulating multiple pathways, such as down‐regulation of EEF1E1, promotion of abnormal lipid metabolism, and up‐regulation of sphingosine kinase 1. Pertinent to clinical practice, a genetic variant in the HULC gene has been found to alter the risk for hepatocellular carcinoma and oesophageal cancer, whereas cancer patients with high or low expression of HULC exhibit different clinical outcome. These findings highlighted the pathogenic role and clinical utility of HULC in human cancers. Further efforts are warranted to promote the development of HULC‐directed therapeutics.
Highly up-regulated in liver cancer (HULC) was originally identified as the most overexpressed long non-coding RNA in hepatocellular carcinoma. Since its discovery, the aberrant up-regulation of HULC has been demonstrated in other cancer types, including gastric cancer, pancreatic cancer, osteosarcoma and hepatic metastasis of colorectal cancer. Recent discoveries have also shed new light on the upstream molecular mechanisms underlying HULC deregulation. As an oncogene, HULC promotes tumorigenesis by regulating multiple pathways, such as down-regulation of EEF1E1, promotion of abnormal lipid metabolism, and up-regulation of sphingosine kinase 1. Pertinent to clinical practice, a genetic variant in the HULC gene has been found to alter the risk for hepatocellular carcinoma and oesophageal cancer, whereas cancer patients with high or low expression of HULC exhibit different clinical outcome. These findings highlighted the pathogenic role and clinical utility of HULC in human cancers. Further efforts are warranted to promote the development of HULC-directed therapeutics.Highly up-regulated in liver cancer (HULC) was originally identified as the most overexpressed long non-coding RNA in hepatocellular carcinoma. Since its discovery, the aberrant up-regulation of HULC has been demonstrated in other cancer types, including gastric cancer, pancreatic cancer, osteosarcoma and hepatic metastasis of colorectal cancer. Recent discoveries have also shed new light on the upstream molecular mechanisms underlying HULC deregulation. As an oncogene, HULC promotes tumorigenesis by regulating multiple pathways, such as down-regulation of EEF1E1, promotion of abnormal lipid metabolism, and up-regulation of sphingosine kinase 1. Pertinent to clinical practice, a genetic variant in the HULC gene has been found to alter the risk for hepatocellular carcinoma and oesophageal cancer, whereas cancer patients with high or low expression of HULC exhibit different clinical outcome. These findings highlighted the pathogenic role and clinical utility of HULC in human cancers. Further efforts are warranted to promote the development of HULC-directed therapeutics.
Highly up‐regulated in liver cancer ( HULC ) was originally identified as the most overexpressed long non‐coding RNA in hepatocellular carcinoma. Since its discovery, the aberrant up‐regulation of HULC has been demonstrated in other cancer types, including gastric cancer, pancreatic cancer, osteosarcoma and hepatic metastasis of colorectal cancer. Recent discoveries have also shed new light on the upstream molecular mechanisms underlying HULC deregulation. As an oncogene, HULC promotes tumorigenesis by regulating multiple pathways, such as down‐regulation of EEF 1E1, promotion of abnormal lipid metabolism, and up‐regulation of sphingosine kinase 1. Pertinent to clinical practice, a genetic variant in the HULC gene has been found to alter the risk for hepatocellular carcinoma and oesophageal cancer, whereas cancer patients with high or low expression of HULC exhibit different clinical outcome. These findings highlighted the pathogenic role and clinical utility of HULC in human cancers. Further efforts are warranted to promote the development of HULC ‐directed therapeutics.
Author Yu, Xin
Wu, William Ka Kei
Zheng, Heyi
Chan, Matthew T.V.
AuthorAffiliation 3 State Key Laboratory of Digestive Disease LKS Institute of Health Sciences The Chinese University of Hong Kong Hong Kong China
1 Department of Dermatology Peking Union Medical College Hospital Chinese Academy of Medical Sciences and Peking Union Medical College Beijing China
2 Department of Anaesthesia and Intensive Care The Chinese University of Hong Kong Hong Kong China
AuthorAffiliation_xml – name: 2 Department of Anaesthesia and Intensive Care The Chinese University of Hong Kong Hong Kong China
– name: 1 Department of Dermatology Peking Union Medical College Hospital Chinese Academy of Medical Sciences and Peking Union Medical College Beijing China
– name: 3 State Key Laboratory of Digestive Disease LKS Institute of Health Sciences The Chinese University of Hong Kong Hong Kong China
Author_xml – sequence: 1
  givenname: Xin
  surname: Yu
  fullname: Yu, Xin
  organization: Chinese Academy of Medical Sciences and Peking Union Medical College
– sequence: 2
  givenname: Heyi
  surname: Zheng
  fullname: Zheng, Heyi
  email: Zhenghy62@sina.com
  organization: Chinese Academy of Medical Sciences and Peking Union Medical College
– sequence: 3
  givenname: Matthew T.V.
  surname: Chan
  fullname: Chan, Matthew T.V.
  organization: The Chinese University of Hong Kong
– sequence: 4
  givenname: William Ka Kei
  surname: Wu
  fullname: Wu, William Ka Kei
  organization: The Chinese University of Hong Kong
BackLink https://www.ncbi.nlm.nih.gov/pubmed/27781386$$D View this record in MEDLINE/PubMed
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Copyright 2016 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.
2017. This work is published under https://creativecommons.org/licenses/by/4.0/ (the "License"). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.
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Issue 2
Keywords cancer
long non-coding RNAs
oncogene
prognosis
HULC
Language English
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PublicationCentury 2000
PublicationDate February 2017
PublicationDateYYYYMMDD 2017-02-01
PublicationDate_xml – month: 02
  year: 2017
  text: February 2017
PublicationDecade 2010
PublicationPlace England
PublicationPlace_xml – name: England
– name: Chichester
– name: Hoboken
PublicationTitle Journal of cellular and molecular medicine
PublicationTitleAlternate J Cell Mol Med
PublicationYear 2017
Publisher John Wiley & Sons, Inc
John Wiley and Sons Inc
Publisher_xml – name: John Wiley & Sons, Inc
– name: John Wiley and Sons Inc
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Snippet Highly up‐regulated in liver cancer (HULC) was originally identified as the most overexpressed long non‐coding RNA in hepatocellular carcinoma. Since its...
Highly up‐regulated in liver cancer ( HULC ) was originally identified as the most overexpressed long non‐coding RNA in hepatocellular carcinoma. Since its...
Highly up-regulated in liver cancer (HULC) was originally identified as the most overexpressed long non-coding RNA in hepatocellular carcinoma. Since its...
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StartPage 410
SubjectTerms Angiogenesis
Biomarkers
Bone cancer
cancer
Carcinogenesis - genetics
Cell growth
Cholesterol
Colorectal cancer
Colorectal carcinoma
Drug development
Esophageal cancer
Esophagus
Gastric cancer
Gene expression
Gene Expression Regulation, Neoplastic
Genetic diversity
Hepatitis
Hepatitis B
Hepatitis B virus - physiology
Hepatocellular carcinoma
HULC
Humans
Hyperplasia
Kinases
Lipid metabolism
Liver cancer
long non‐coding RNAs
Lymphatic system
Metastases
Metastasis
Models, Biological
Molecular modelling
Neoplasms - genetics
Non-coding RNA
oncogene
Osteosarcoma
Pancreatic cancer
prognosis
Proteins
Review
Ribonucleic acid
RNA
RNA, Long Noncoding - genetics
RNA, Long Noncoding - metabolism
Sarcoma
Sphingosine kinase
Stem cells
Studies
Transcription factors
Tumorigenesis
Tumors
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Title HULC: an oncogenic long non‐coding RNA in human cancer
URI https://onlinelibrary.wiley.com/doi/abs/10.1111%2Fjcmm.12956
https://www.ncbi.nlm.nih.gov/pubmed/27781386
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