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

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===Characteristics===
 
===Characteristics===
−
Bidirectional transcript from the CDKN1A promoter.
+
The PANDAR was located approximately 5 kilobases upstream of the CDKN1A transcription start site and was induced upon DNA damage. <ref name="ref1" />
  
−
1.5kb single exon.
 
  
 
Sequence runs antisense through a processed LAP3 pseudogene and contains a SINE.
 
Sequence runs antisense through a processed LAP3 pseudogene and contains a SINE.
  
 
===Function===
 
===Function===
−
P53 effector gene, acts in response to DNA damage to limit apoptosis while CDKN1A induces cell cycle arrest.
+
[[File:''PANDA'' regulates transcription factor NF-YA.jpgright|thumb|400px|'''''PANDA'' regulates transcription factor NF-YA.'''<ref name="ref1" />]]
 +
''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.<ref name="ref1" />
 +
[[File:''PANDA'' regulates transcription factor NF-YA.jpgright|thumb|400px|'''''PANDA'' regulates transcription factor NF-YA.'''<ref name="ref1" />]]
 +
DNA damage activates p53-mediated transcription at ''CDKN1A'' and ''PANDA'' that functions synergistically to mediate cell cycle arrest and survival.<ref name="ref1" />
  
−
Loss of PANDA leads to the apoptosis of doxorubicin treated cells.
+
''PANDAR'' could function as a tumor-promoting gene in breast cancer by regulating G1/S transition. <ref name="ref2" />
 +
===Expression===
 +
[[File:''PANDAR'' was dysregulated in breast cancer.jpgright|thumb|400px|'''''PANDAR'' was dysregulated in breast cancer.'''<ref name="ref1" />]]
  
−
Loss of PANDA affected the expression of many genes during the DNA damage response. Upregulated genes were enriched for those involved in apoptosis, including the apoptotic activators APAF1, BIK, FAS and LRDD. Leading to apoptosis of doxorubicin treated cells.
+
''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.<ref name="ref1" />
 +
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.<ref name="ref1" />
  
−
Cell death genes downstream of p53 are known to have NF-YA binding sites. PANDA RNA interacts with the transcription factor NF-YA and attenuates its occupany of target gene promoters.
+
Expression of ''PANDA'' and ''CDKN1A'' were positively regulated by p53.<ref name="ref1" />
  
−
===Expression===
+
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.<ref name="ref1" />
−
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.
+
 
 +
''PANDAR'' is up-regulated in breast cancer clinical samples as well as cell lines.<ref name="ref2" />
 +
 
 +
''PANDAR'' enhanced the binding of Bim1 complex to p16INK4A promoter and suppressed p16INK4A expression.<ref name="ref2" />
 +
 
 +
{|class='wikitable' style="text-align:center"
 +
|-
 +
! | Primers
 +
! | Fwd
 +
! | Rev
 +
|-
 +
| | Primers used in RACE
 +
| | 5'-CAGAACTTGGCATGATGGAG-3'
 +
5'-TGCACACATTTAACCCGAAG-3'<ref name="ref1" />
 +
| | 5'-TGATATGAAACTCGGTTTACTACTAGC-3'
 +
5'-CCCCAAAGCTACATCTATGACA-3'
  
−
Induced up to 40 fold upon DNA damage peaking 16 h after doxorubicin treatment, a much greater response than shown by CDKN1A.
+
5'-CGTCTCCATCAT GCCAAGTT-3'
  
−
Expression of PANDA and CDKN1A were positively regulated by p53. CDKN1A did not induce PANDA.
+
5'-CATAGAGCTTCACCGACATAGC-3'<ref name="ref1" />
 +
|-
 +
| rowspan="1"|RT-PCR primers for PANDAR
 +
| | 5'-TGCACACATTTAACCCGAAG-3'
 +
| | 5'-CCCCAAAGCTACATCTATGACA-3'<ref name="ref1" /><ref name="ref2" />
 +
|-
 +
| rowspan="3"|siRNAs for PANDAR
 +
| | 5'-AAUGUGUGCACGUAACAGAUU-3'
 +
| | 5'-GAGAUUUGCAGCAGACACAUU-3'<ref name="ref1" />
 +
|-
 +
| | 5'-GGGCAUGUUUUCACAGAGGUU-3'
 +
| | 5'-GAGAUUUGCAGCAGACACAUU-3'<ref name="ref1" />
 +
|-
 +
| | 5'-AAUGUGUGCACGUAACAGAUU-3'
 +
| | 5'-GGGCAUGUUUUCACAGAGGUU-3'<ref name="ref1" />
 +
|-
 +
| rowspan="1"|ChIP assay
 +
| | 5'-CCCATTTTCCTATCTGC-3'
 +
| | 5'-CTAGTTCAAAGGATTCC-3'<ref name="ref2" />
 +
|}
  
−
===Conservation===
+
===Disease===
−
Syntenic sequence appear to be present in apes and old world monkeys (the Catarrhini).
+
* breast cancer <ref name="ref2" />
  
 
===Misc===
 
===Misc===
Line 40: Line 79:
  
 
===Regulation===
 
===Regulation===
−
Please input regulation information here.
+
During DNA damage, PANDAR is induced by p53. <ref name="ref1" />
  
 
===Allelic Information and Variation===
 
===Allelic Information and Variation===
Line 48: Line 87:
 
Please input evolution information here.
 
Please input evolution information here.
  
−
You can also add sub-section(s) at will.
 
  
 
==Labs working on this lncRNA==
 
==Labs working on this lncRNA==
−
Please input related labs here.
+
* 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" />
  
 
==References==
 
==References==
−
[http://www.lncrnadb.org/PANDA/ Annotation originally sourced from lncRNAdb.]
+
<references>
 +
<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)
 +
<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）
 +
</references>
  
 
{{basic|
 
{{basic|

Revision as of 02:52, 1 July 2016

Please input one-sentence summary here.

Annotated Information

Name

PANDAR:promoter of CDKN1A antisense DNA damage activated RNA

PANDA

Characteristics

The PANDAR was located 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

File:PANDA regulates transcription factor NF-YA.jpgright
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]

File:PANDA regulates transcription factor NF-YA.jpgright
PANDA regulates transcription factor NF-YA.[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]

Expression

File:PANDAR was dysregulated in breast cancer.jpgright
PANDAR was dysregulated in breast cancer.[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] 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]

Disease

  • breast cancer [2]

Misc

Please input misc information here.

Transcriptomic Nomeclature

Please input transcriptomic nomeclature information here.

Regulation

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

Allelic Information and Variation

Please input allelic information and variation information here.

Evolution

Please input evolution information here.


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]

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 1.17 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 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.

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 GCCTGCCT