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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Veröffentlicht in:Journal of cellular and molecular medicine Jg. 21; H. 2; S. 410 - 417
Hauptverfasser: Yu, Xin, Zheng, Heyi, Chan, Matthew T.V., Wu, William Ka Kei
Format: Journal Article
Sprache:Englisch
Veröffentlicht: England John Wiley & Sons, Inc 01.02.2017
John Wiley and Sons Inc
Schlagworte:
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
Online-Zugang:Volltext
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Zusammenfassung: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.
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ISSN:1582-1838
1582-4934
1582-4934
DOI:10.1111/jcmm.12956