Difference between revisions of "Lnc-CDKN1A-1:1"

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Please input one-sentence summary here.
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''PANDAR'': "promoter of CDKN1A antisense DNA damage activated RNA", a long non coding RNA that regulates the response to DNA damage.
  
 
==Annotated Information==
 
==Annotated Information==
 
===Name===
 
===Name===
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PANDAR:promoter of CDKN1A antisense DNA damage activated RNA
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PANDAR:promoter of CDKN1A antisense DNA damage activated RNA [https://www.genenames.org/data/gene-symbol-report/#!/hgnc_id/HGNC:44048 (HGNC:44048)]
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===Alias===
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PANDA
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PANDA: p21 associated ncRNA DNA damage activated [https://www.genenames.org/data/gene-symbol-report/#!/hgnc_id/HGNC:44048 (HGNC:44048)]
  
 
===Characteristics===
 
===Characteristics===
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The PANDAR was located approximately 5 kilobases upstream of the CDKN1A transcription start site and was induced upon DNA damage. <ref name="ref1" />
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The PANDAR is located at chromosome 6p21.2, approximately 5 kilobases upstream of the CDKN1A transcription start site and was induced upon DNA damage. <ref name="ref1" />
  
 
Sequence runs antisense through a processed LAP3 pseudogene and contains a SINE.
 
Sequence runs antisense through a processed LAP3 pseudogene and contains a SINE.
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===Disease===
 
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breast cancer
 
  
 
===Function===
 
===Function===
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''PANDAR'' could function as a tumor-promoting gene in breast cancer by regulating G1/S transition. <ref name="ref2" />
 
''PANDAR'' could function as a tumor-promoting gene in breast cancer by regulating G1/S transition. <ref name="ref2" />
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===Regulation===
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During DNA damage, PANDAR is induced by p53. <ref name="ref1" />
  
 
===Expression===
 
===Expression===
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===Disease===
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===Diseases===
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* breast cancer <ref name="ref2" />
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* Bladder cancer <ref name="ref3" />
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* Breast Cancer <ref name="ref2" />
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===Misc===
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* Gastric cancer <ref name="ref4" />
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Please input misc information here.
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* Hepatocellular carcinoma <ref name="ref5" />
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* Non-small cell lung cancer <ref name="ref6" />
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===Transcriptomic Nomeclature===
 
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===Regulation===
 
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During DNA damage, PANDAR is induced by p53. <ref name="ref1" />
 
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===Allelic Information and Variation===
 
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===Evolution===
 
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==Labs working on this lncRNA==
 
==Labs working on this lncRNA==
 
* Program in Epithelial Biology, Stanford University School of Medicine, Stanford, California, USA.<ref name="ref1" />
 
* Program in Epithelial Biology, Stanford University School of Medicine, Stanford, California, USA.<ref name="ref1" />
 
* Nanchang Key Laboratory of Cancer Pathogenesis and Translational Research, Center Laboratory, the Third Affiliated Hospital, Nanchang University, Nanchang, P.R. China.<ref name="ref2" />
 
* Nanchang Key Laboratory of Cancer Pathogenesis and Translational Research, Center Laboratory, the Third Affiliated Hospital, Nanchang University, Nanchang, P.R. China.<ref name="ref2" />
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* Key Laboratory of Medical Reprogramming Technology, Shenzhen Second People’s Hospital, The First Affiliated Hospital of Shenzhen University Shenzhen, Shenzhen, China. <ref name="ref3" />
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* Department of Oncology, The First Affiliated Hospital of Nanjing Medical University, No.300 Guangzhou Road, Nanjing, Jiangsu 210029, China. <ref name="ref4" />
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* Department of Medical Oncology, Jiangsu Cancer Hospital, Nanjing Medical University, Nanjing, China <ref name="ref5" />
  
 
==References==
 
==References==
 
<references>
 
<references>
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<ref name="ref1">Hung T, Wang Y, Lin MF, Koegel AK, Kotake Y, Grant GD, et al. Extensive and coordinated transcription of noncoding RNAs within cell-cycle promoters[J]. Nature genetics. 2011,43(7):621-9.</ref>(1)
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<ref name="ref1"> Hung T, Wang Y, Lin MF, Koegel AK, Kotake Y, Grant GD, et al. Extensive and coordinated transcription of noncoding RNAs within cell-cycle promoters[J]. Nature genetics. 2011,43(7):621-9.</ref>(1)
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<ref name="ref2">Sang Y, Tang J, Li S, Li L, Tang X, Cheng C, et al. LncRNA PANDAR regulates the G1/S transition of breast cancer cells by suppressing p16(INK4A) expression[J]. Scientific reports. 2016,6:22366.</ref>(2）
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<ref name="ref2"> Sang Y, Tang J, Li S, Li L, Tang X, Cheng C, et al. LncRNA PANDAR regulates the G1/S transition of breast cancer cells by suppressing p16(INK4A) expression[J]. Scientific reports. 2016,6:22366.</ref>(2)
 +
<ref name="ref3"> Zhan Y, Lin J, Liu Y, Chen M, Chen X, Zhuang C et al. Up-regulation of long non-coding RNA PANDAR is associated with poor prognosis and promotes tumorigenesis in bladder cancer[J]. Journal of Experimental & Clinical Cancer Research. 2016, 35(1):83.</ref>(3)
 +
<ref name="ref4"> Ma P, Xu T, Huang M & Shu Y. Increased expression of LncRNA PANDAR predicts a poor prognosis in gastric cancer[J]. Biomedicine & Pharmacotherapy. 2016, 78:172-176.</ref>(4)
 +
<ref name="ref5"> Peng W & Fan H. Long non-coding RNA PANDAR correlates with poor prognosis and promotes tumorigenesis in hepatocellular carcinoma[J]. Biomedicine & Pharmacotherapy. 2015, 72:113-118.</ref>(5)
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<ref name="ref6"> Han L, Zhang Eb, Yin Dd, Kong R, Xu Tp, Chen Wm et al. Low expression of long noncoding RNA PANDAR predicts a poor prognosis of non-small cell lung cancer and affects cell apoptosis by regulating Bcl-2[J]. Cell Death &Amp; Disease. 2015, 6:e1665.</ref>(6)
 
</references>
 
</references>
  

Latest revision as of 09:27, 21 November 2018

PANDAR: "promoter of CDKN1A antisense DNA damage activated RNA", a long non coding RNA that regulates the response to DNA damage.

Annotated Information

Name

PANDAR:promoter of CDKN1A antisense DNA damage activated RNA (HGNC:44048)

Alias

PANDA: p21 associated ncRNA DNA damage activated (HGNC:44048)

Characteristics

The PANDAR is located at chromosome 6p21.2, approximately 5 kilobases upstream of the CDKN1A transcription start site and was induced upon DNA damage. [1]

Sequence runs antisense through a processed LAP3 pseudogene and contains a SINE.

Function

PANDA regulates transcription factor NF-YA.[1]

PANDA interacts with the transcription factor NF-YA to limit expression of pro-apoptotic genes; PANDA depletion markedly sensitized human fibroblasts to apoptosis by doxorubicin.[1]

Model of coding and noncoding transcripts at the CDKN1A locus coordinating the DNA damage response.[1]

DNA damage activates p53-mediated transcription at CDKN1A and PANDA that functions synergistically to mediate cell cycle arrest and survival.[1]

PANDAR could function as a tumor-promoting gene in breast cancer by regulating G1/S transition. [2]

Regulation

During DNA damage, PANDAR is induced by p53. [1]

Expression

PANDAR was dysregulated in breast cancer.[2]

PANDA interacts with the transcription factor NF-YA to limit expression of pro-apoptotic genes; PANDA depletion markedly sensitized human fibroblasts to apoptosis by doxorubicin.[1] One of five lncRNAs surrounding the transcription start site of the cell cycle gene CDKN1A that, along with the CDKN1A protein coding gene, were induced in human fetal lung fibroblasts upon DNA damage by doxorubicin.[1]

Expression of PANDA and CDKN1A were positively regulated by p53.[1]

Expression of neither CDKN1A itself nor TP53 was affected by PANDA depletion, suggesting that PANDA is a P53 effector that acts independently of p21-CDKN1A.[1]

PANDAR is up-regulated in breast cancer clinical samples as well as cell lines.[2]

PANDAR enhanced the binding of Bim1 complex to p16INK4A promoter and suppressed p16INK4A expression.[2]

Primers Fwd Rev
Primers used in RACE 5'-CAGAACTTGGCATGATGGAG-3'

5'-TGCACACATTTAACCCGAAG-3'[1]

5'-TGATATGAAACTCGGTTTACTACTAGC-3'

5'-CCCCAAAGCTACATCTATGACA-3'

5'-CGTCTCCATCAT GCCAAGTT-3'

5'-CATAGAGCTTCACCGACATAGC-3'[1]

RT-PCR primers for PANDAR 5'-TGCACACATTTAACCCGAAG-3' 5'-CCCCAAAGCTACATCTATGACA-3'[1][2]
siRNAs for PANDAR 5'-AAUGUGUGCACGUAACAGAUU-3' 5'-GAGAUUUGCAGCAGACACAUU-3'[1]
5'-GGGCAUGUUUUCACAGAGGUU-3' 5'-GAGAUUUGCAGCAGACACAUU-3'[1]
5'-AAUGUGUGCACGUAACAGAUU-3' 5'-GGGCAUGUUUUCACAGAGGUU-3'[1]
ChIP assay 5'-CCCATTTTCCTATCTGC-3' 5'-CTAGTTCAAAGGATTCC-3'[2]

Diseases

  • Bladder cancer [3]
  • Breast Cancer [2]
  • Gastric cancer [4]
  • Hepatocellular carcinoma [5]
  • Non-small cell lung cancer [6]

Labs working on this lncRNA

  • Program in Epithelial Biology, Stanford University School of Medicine, Stanford, California, USA.[1]
  • Nanchang Key Laboratory of Cancer Pathogenesis and Translational Research, Center Laboratory, the Third Affiliated Hospital, Nanchang University, Nanchang, P.R. China.[2]
  • Key Laboratory of Medical Reprogramming Technology, Shenzhen Second People’s Hospital, The First Affiliated Hospital of Shenzhen University Shenzhen, Shenzhen, China. [3]
  • Department of Oncology, The First Affiliated Hospital of Nanjing Medical University, No.300 Guangzhou Road, Nanjing, Jiangsu 210029, China. [4]
  • Department of Medical Oncology, Jiangsu Cancer Hospital, Nanjing Medical University, Nanjing, China [5]

References

  1. ↑ 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 1.15 1.16 Hung T, Wang Y, Lin MF, Koegel AK, Kotake Y, Grant GD, et al. Extensive and coordinated transcription of noncoding RNAs within cell-cycle promoters[J]. Nature genetics. 2011,43(7):621-9.
  2. ↑ 2.0 2.1 2.2 2.3 2.4 2.5 2.6 2.7 Sang Y, Tang J, Li S, Li L, Tang X, Cheng C, et al. LncRNA PANDAR regulates the G1/S transition of breast cancer cells by suppressing p16(INK4A) expression[J]. Scientific reports. 2016,6:22366.
  3. ↑ 3.0 3.1 Zhan Y, Lin J, Liu Y, Chen M, Chen X, Zhuang C et al. Up-regulation of long non-coding RNA PANDAR is associated with poor prognosis and promotes tumorigenesis in bladder cancer[J]. Journal of Experimental & Clinical Cancer Research. 2016, 35(1):83.
  4. ↑ 4.0 4.1 Ma P, Xu T, Huang M & Shu Y. Increased expression of LncRNA PANDAR predicts a poor prognosis in gastric cancer[J]. Biomedicine & Pharmacotherapy. 2016, 78:172-176.
  5. ↑ 5.0 5.1 Peng W & Fan H. Long non-coding RNA PANDAR correlates with poor prognosis and promotes tumorigenesis in hepatocellular carcinoma[J]. Biomedicine & Pharmacotherapy. 2015, 72:113-118.
  6. ↑ Han L, Zhang Eb, Yin Dd, Kong R, Xu Tp, Chen Wm et al. Low expression of long noncoding RNA PANDAR predicts a poor prognosis of non-small cell lung cancer and affects cell apoptosis by regulating Bcl-2[J]. Cell Death &Amp; Disease. 2015, 6:e1665.

Basic Information

Transcript ID

lnc-CDKN1A-1:1

Source

LNCipedia2.1

Same with

,

Classification

intergenic

Length

1506 nt

Genomic location

chr6+:36641397..36642903

Exon number

,

Exons

,

Genome context

Sequence
000001 ACGAATTCTT TCAGGAATGC CGCAGATGTA CATGCTCCCG CAGATCTATA TTTTCCAATG TTGTTAACAT CAGCCAGCTG 000080
000081 GCAATCTACA ACCTGTCTTG TACAATGTTT GAAGAGAGGC ATCCTCCAGA CACGGTCCCC TGTTTCAATG CTGGCCTCGA 000160
000161 AGAGCTTGTT CCAGAGCCAG GATGAATTGG TAAAGACCCC AGTGGCACCT GACCCCAAAG CTACATCTAT GACACCTGTT 000240
000241 AAGGTGGTGG CATTGAGGAT GACCTTCGGG TTAAATGTGT GCACGTAACA GAGCGCATCA GCCAGTATGA GCCTCCCCTC 000320
000321 AGCATCAGTG TTACCAACCT GGATGGTCTT CCTGTTCCTG GCTCTAACAA CATCCCCCAG CTTGTTGGCC TTGCCGCTGG 000400
000401 GCATGTTTTC ACAGAGGGGC CAGACCTATA ATATTAATGG GCAAACTGAG ATTTGCAGCA GACACAATGG CTGAGCATAT 000480
000481 AGTTGTAGCT CCTCCCATGT CGGCCCTCAT GAGGTCCATA TTTGCAGAAG CCTTGATGGA GATACCACCA CTGTCAAAGG 000560
000561 TAATTCCTTT CCCAACAAAC AAGGGGTGGT TTGTCTGCAT TGGGGCTGCC TATGTAGTGA ATTTCCAAGA AGACTGAGGG 000640
000641 CTCGTCAGAT CCTTTGGCCA CACTGAGGAA TGATCCCATT GCCTGTTCCT CAATCCAAGA CCTGGGTCTG ATATGAAACT 000720
000721 CGGTTTACTA CTAGCGCTTT TGAGATTCTT CTCAATAATT TCGGCAAATC TGGTTGGCAT CATCTCGCTG GCTGGCGTCT 000800
000801 CCATCATGCC AAGTTCTGCC CAGAAGCAAA CAGGACTCCT TTCTGCCAGG CCTCCTGATC CCCAGTTCCA TAGAGCTTCA 000880
000881 CCGACATAGC CATCTTCTTT TTTTGCTTTA GGTCATCGTA TTCATAGAGA CCAAGCACCG CGCCCTCCTC AGCAGCCTGA 000960
000961 GCATCTCTAC AGGGATCCAC CTCCACGGAA GAGAGCTCCA GGTCTTGAAT CTGCCTGCAT CCTGCTGCAA CAGCAGCTCT 001040
001041 GATGTTTTCT TTGCCTTCCT GCCAGTTTTC CTGTTCGTCG ATTCTGGCTG CCTTTTTGCC GAGGCCAACT AGCACCACGC 001120
001121 TGGGGAAGTC CTGATGCAGA CCATAAAAGT TTCGAGTCTT GCCTGCCTTC AGAGGTGGTC CAGATATGTT CAAAGTCTCT 001200
001201 CTCAGCTTTC CAGCTATCAA TTTATCAAGA TTCTCTCCTG CACTTGTGAA CTGTGGCACA TCATC