Difference between revisions of "NR4A1AS"
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NR4A1AS up-regulates NR4A1 expression by forming RNA-RNA complexes and blocking UPF1-mediated mRNA destabilization<ref name="ref1" /> | NR4A1AS up-regulates NR4A1 expression by forming RNA-RNA complexes and blocking UPF1-mediated mRNA destabilization<ref name="ref1" /> | ||
===Expression=== | ===Expression=== | ||
| − | [[File: NR4A1AS. | + | [[File: NR4A1AS.jpg|thumb|550px|NR4A1 expression is increased in colorectal cancer (CRC) tissues and cells.<ref name="ref1"/>]] |
| − | NR4A1AS stabilized NR4A1 mRNA by forming RNA-RNA complexes via partial base-pairing and up-regulated NR4A1 expression in CRC cells.<ref name="ref1" /> | + | NR4A1AS stabilized NR4A1 mRNA by forming RNA-RNA complexes via partial base-pairing and up-regulated NR4A1 expression in CRC cells.<ref name="ref1" /> |
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===Diseases=== | ===Diseases=== | ||
Colorectal cancer<ref name="ref1" /> | Colorectal cancer<ref name="ref1" /> | ||
Revision as of 01:11, 19 February 2021
NR4A1AS，an antisense lncRNA of NR4A1，is involved in colorectal cancer (CRC) development.[1]
Contents
Annotated Information
Name
Approved symbol:NR4A1AS
Approved name:NR4A1 antisense RNA
HGNC ID HGNC:54409
Alias symbol:NR4A1-AS1
RefSeq ID:NR_170321
Characteristics
NR4A1AS located in the same primary transcript harboring miR-23a 27a 24-2 cluster is a stable, nuclear restricted and chromatin associated lncRNA.[1]
Function
NR4A1AS can make cell proliferation, migration and invasion.[1] NR4A1AS functions in tumor growth and metastasis of CRC cells at least partly through regulating NR4A1.[1]
Regulation
NR4A1AS up-regulates NR4A1 expression by forming RNA-RNA complexes and blocking UPF1-mediated mRNA destabilization[1]
Expression
File:NR4A1AS.jpg
NR4A1 expression is increased in colorectal cancer (CRC) tissues and cells.[1]
NR4A1AS stabilized NR4A1 mRNA by forming RNA-RNA complexes via partial base-pairing and up-regulated NR4A1 expression in CRC cells.[1]
Diseases
Colorectal cancer[1]
Labs working on this lncRNA
- Guangdong Key Laboratory of Systems Biology and Synthetic Biology for Urogenital Tumors, Institute of Translational Medicine, First Affiliated Hospital of Shenzhen University, Shenzhen Second People's Hospital, Shenzhen 518035, China.[1]
- Department of Cell Biology and Genetics, Key Laboratory of Molecular Biology in High Cancer Incidence Coastal Chaoshan Area of Guangdong Higher Education Institutes, Shantou University Medical College, Shantou 515041, China.[1]
- Department of Minimally Invasive Intervention, Peking University Shenzhen Hospital, Shenzhen 518036, China.[1]
- Department of Pathology, Shenzhen People's Hospital, Shenzhen 518000, China.[1]
- Department of Pathology and Central Laboratory, Shantou Central Hospital, Affiliated Shantou Hospital of Sun Yat-sen University, Shantou 515041, China.[1]
- Department of Urinary Surgery, Shenzhen Second People's Hospital, The First Affiliated Hospital of Shenzhen University, Health Science Center, Shenzhen 518035, China.[1]
- Department of General Surgery, First Affiliated Hospital of Shantou University Medical College, Shantou 515041, China.[1]
- Department of Cell Biology and Genetics, Key Laboratory of Molecular Biology in High Cancer Incidence Coastal Chaoshan Area of Guangdong Higher Education Institutes, Shantou University Medical College, Shantou 515041, China tangaifa2018@email.szu.edu.cn huangdy@stu.edu.cn.</ref>(1)
- Guangdong Key Laboratory of Systems Biology and Synthetic Biology for Urogenital Tumors, Institute of Translational Medicine, First Affiliated Hospital of Shenzhen University, Shenzhen Second People's Hospital, Shenzhen 518035, China tangaifa2018@email.szu.edu.cn huangdy@stu.edu.cn.</ref>(1)
References
- ↑ 1.00 1.01 1.02 1.03 1.04 1.05 1.06 1.07 1.08 1.09 1.10 1.11 1.12 1.13 1.14 Xie X, Lin J, Liu J, Huang M, Zhong Y, Liang B, Song X, Gu S, Chang X, Huang D, Tang A. A novel lncRNA NR4A1AS up-regulates orphan nuclear receptor NR4A1 expression by blocking UPF1-mediated mRNA destabilization in colorectal cancer. Clin Sci (Lond). 2019 Jul 15;133(13):1457-1473. doi: 10.1042/CS20181061.
