Difference between revisions of "FEZF1-AS1"

From LncRNAWiki
Jump to: navigation, search
(→‎Annotated Information)
 
(3 intermediate revisions by one other user not shown)
Line 1: Line 1:
 
==Annotated Information==
 
==Annotated Information==
 
===Name===
 
===Name===
−
FEZF1-AS1:FEZF1 antisense RNA 1<ref name="ref1" />
+
Approved symbol: FEZF1-AS1:FEZF1 antisense RNA 1<ref name="ref1" />
 +
 
 +
HGNC ID: HGNC:41001
 +
 
 +
Ensembl ID: ENSG00000230316
 +
 
 +
RefSeq ID: NR_036484
 +
 
 +
LncBook transcript ID: HSALNT0288975
  
 
===Characteristics===
 
===Characteristics===
−
FEZF1-AS1 is a conserved ~2.6-kb RNA transcribed from the plus strand of chromosome 7, on the opposite strand of the gene coding FEZF1 protein (7q31.32), including 611 nucleotides of full complementarity between the frst FEZF1-AS1 exon and FEZF1 exons 1 <ref name="ref1" />.
+
FEZF1-AS1 is a ~2.6-kb RNA transcribed from the plus strand of chromosome 7 <ref name="ref1" /><ref name="ref2" />. FEZF1-AS1 is transcribed from the opposite strand of FEZF1 protein (7q31.32), and there are 611 nucleotides of full complementarity between the frst FEZF1-AS1 exon and FEZF1 exons 1 <ref name="ref1" />.
−
FEZF1-AS1 is a lncRNA producing a 2564 bp transcript, located in chromosome 7<ref name="ref2" />.
 
−
 
 
−
It belongs to the category of "Antisense" in lncRNA classification.
 
−
===Cellular Localization===
 
−
7q31.32
 
  
 
===Function===
 
===Function===
 
[[File:FEZF1-AS1-1.JPG|right|thumb|400px|'''''FEZF1-AS1''''' regulates GC cell proliferation<ref name="ref2" />.]]
 
[[File:FEZF1-AS1-1.JPG|right|thumb|400px|'''''FEZF1-AS1''''' regulates GC cell proliferation<ref name="ref2" />.]]
  
−
Downregulation of FEZF1-AS1 expression will signifcantly inhibit the CRC cells proliferation, migration and invasiveness, suppress S-phase entry in vitro, repress tumor growth and metastasis in vivo, and also reduce its sense-cognate gene FEZF1 mRNA and protein expression in CRC cells<ref name="ref1" />.
+
*Dysregulation of FEZF1-AS1 participates in colorectal tumorigenesis and progression, which might be achieved, at least in part, through FEZF1 induction <ref name="ref1" />.
 +
 
 +
*FEZF1-AS1 could act as an "oncogene" for gastric cancer partly through suppressing P21 expression; FEZF1-AS1 may be served as a candidate prognostic biomarker and target for new therapies of gastric cancer patients <ref name="ref2" />. FEZF1-AS1 is overexpressed in gastric cancer, and upregulated FEZF1-AS1 expression is correlated with larger tumor size and higher clinical stage; additional higher expression of FEZF1-AS1 predicted poor prognosis <ref name="ref2" />. FEZF1-AS1 could epigenetically repress the expression of P21 via binding with LSD1 (a demethylase) <ref name="ref2" />.
  
−
FEZF1-AS1 boost gastric cancer cell proliferation:(I) SP1 accelerated FEZF1-AS1 overexpressioon in gastric cancer; (II) FEZF1 -AS1 caused G1-S arrest contributing to proliferation; (III) FEZF1 -AS1 repressed p21 transcription by recruiting LSD1 causing H3K4me2 demethylation at the p21 promoter in gastric cancer.  
+
[[File:FEZF1-AS1-fun.png|right|thumb|400px|An illustrative figure detailing the relationship among FEZF1-AS1, miR-610 and Akt3.<ref name="ref3" />.]]
−
FEZF1-AS1 promoted gastric cancer cell proliferation and tumorigenesis in vivio and vivo by affecting cell cycle progression.<ref name="ref2" />.  
+
*FEZF1-AS1 inhibition reduced myeloma (MM) cells proliferation, arrested cell cycle in G0/G1 phase and induced cell apoptosis. Furthermore, FEZF1-AS1 promoted MM cells progression by regulating miR-610/Akt3 axis<ref name="ref3" />.
 +
 
 +
===Expression===
 +
FEZF1-AS1 is overexpressed in gastric cancer, and upregulated FEZF1-AS1 expression is correlated with larger tumor size and higher clinical stage; additional higher expression of FEZF1-AS1 predicted poor prognosis <ref name="ref2" />.
 +
 
 +
Expression of FEZF1-AS1 was upregulated in myeloma (MM) samples and cell lines<ref name="ref3" />.
  
 
===Disease===
 
===Disease===
 
*Colorectal carcinoma<ref name="ref1" />
 
*Colorectal carcinoma<ref name="ref1" />
 
*Gastric cancer<ref name="ref2" />
 
*Gastric cancer<ref name="ref2" />
−
 
+
*Myeloma (MM)
  
 
===Sequence===
 
===Sequence===
Line 87: Line 97:
 
<ref name="ref2">
 
<ref name="ref2">
 
Liu YW, Xia R, Lu K, Xie M, Yang F, Sun M, De W, Wang C, Ji G.
 
Liu YW, Xia R, Lu K, Xie M, Yang F, Sun M, De W, Wang C, Ji G.
−
LincRNAFEZF1-AS1 represses p21 expression to promote gastric cancer proliferation
+
LincRNAFEZF1-AS1 represses p21 expression to promote gastric cancer proliferation through LSD1-Mediated H3K4me2 demethylation. Mol Cancer. 2017 Feb 16;16(1):39.
−
through LSD1-Mediated H3K4me2 demethylation. Mol Cancer. 2017 Feb 16;16(1):39.
+
</ref>
 +
<ref name="ref3">
 +
Li QY, Chen L, Hu N, Zhao H. Long non-coding RNA FEZF1-AS1 promotes cell growth in multiple myeloma via miR-610/Akt3 axis. Biomed Pharmacother. 2018 Jul;103:1727-1732.
 
</ref>
 
</ref>
 
</references>
 
</references>

Latest revision as of 01:31, 14 August 2019

Annotated Information

Name

Approved symbol: FEZF1-AS1:FEZF1 antisense RNA 1[1]

HGNC ID: HGNC:41001

Ensembl ID: ENSG00000230316

RefSeq ID: NR_036484

LncBook transcript ID: HSALNT0288975

Characteristics

FEZF1-AS1 is a ~2.6-kb RNA transcribed from the plus strand of chromosome 7 [1][2]. FEZF1-AS1 is transcribed from the opposite strand of FEZF1 protein (7q31.32), and there are 611 nucleotides of full complementarity between the frst FEZF1-AS1 exon and FEZF1 exons 1 [1].

Function

FEZF1-AS1 regulates GC cell proliferation[2].
  • Dysregulation of FEZF1-AS1 participates in colorectal tumorigenesis and progression, which might be achieved, at least in part, through FEZF1 induction [1].
  • FEZF1-AS1 could act as an "oncogene" for gastric cancer partly through suppressing P21 expression; FEZF1-AS1 may be served as a candidate prognostic biomarker and target for new therapies of gastric cancer patients [2]. FEZF1-AS1 is overexpressed in gastric cancer, and upregulated FEZF1-AS1 expression is correlated with larger tumor size and higher clinical stage; additional higher expression of FEZF1-AS1 predicted poor prognosis [2]. FEZF1-AS1 could epigenetically repress the expression of P21 via binding with LSD1 (a demethylase) [2].
An illustrative figure detailing the relationship among FEZF1-AS1, miR-610 and Akt3.[3].
  • FEZF1-AS1 inhibition reduced myeloma (MM) cells proliferation, arrested cell cycle in G0/G1 phase and induced cell apoptosis. Furthermore, FEZF1-AS1 promoted MM cells progression by regulating miR-610/Akt3 axis[3].

Expression

FEZF1-AS1 is overexpressed in gastric cancer, and upregulated FEZF1-AS1 expression is correlated with larger tumor size and higher clinical stage; additional higher expression of FEZF1-AS1 predicted poor prognosis [2].

Expression of FEZF1-AS1 was upregulated in myeloma (MM) samples and cell lines[3].

Disease

  • Colorectal carcinoma[1]
  • Gastric cancer[2]
  • Myeloma (MM)

Sequence

>NR_036484.1 Homo sapiens FEZF1 antisense RNA 1 (FEZF1-AS1), long non-coding RNA

000001 GAAAACTTTG GGCTTGGCAT TAGGAGAGCC TCGGCTGAAA TCCGAGGTTT TGAACGCGAT TTTTTCCGAC AGAAGCTGGG 000080
000081 CGCTTTCTTT CATGTAATGC TGCAGCTGAG CCTGGGACAG GTCTTTGAAA GCTACTCCAG AAGGGTATTT CTCCACCGCC 000160
000161 GGGACCACCA GTTTATTCCT TTCGGCTAAA TACGTTTTTG GCTGCGGGTG CAAAGGGGAA CTGAGGAAGT AGGAGGCCAC 000240
000241 CGGGTGGATG TTCACGCCGG CTGCCGGGTG GCATGGGCCG TCACCTCGGT TCAGGTAGCA CAAGGCGCCC ATGGCGTGGA 000320
000321 ATGAAGAGTG GTTGACCACA CGCGGCCTTA CCAGCTTGTA CTGCTGCAGC GGCAGCGCGT CGCGGGCCAG GTCGCCCTTG 000400
000401 AGACTCAGTG CGCAGTTGAG CAGGTCGCTG CAGCTGAATG CGGGAGCCGA GGGCACCGCC GCGGGCGCCG CCGGGGCCTC 000480
000481 CAGACTGGCC TTCCGCGGCT CGGAGCCCGT CACTCCTGCC TTGGGGCTCG TGTCGTAGGC CACAGGCACG AAGGGGATCA 000560
000561 TGCAGGGGAT CGACGAGTTG AGATGCAGAG AGTGCTTGGG TTCCCCCTTG GCATCACCAG CCGAACCTGC CTGCCCAGCC 000640
000641 CAATGGACTC CTGCCAGCCC ATCGCAGAGT TCTTGGCGCA CCAATGACTC GGGGACAATC ACTACTTATT TCTATCAATA 000720
000721 GAAAGTGTTG TGTCAATAAC GCAGCCAAGA TCTCGCCAAT CGTTAACTTC CAAGAGGAGA AGGGCTCGGG GTTGCCCGCT 000800
000801 CCCGGAATCC CGGAGTCTCC GCGGCCCGAA CCGAGTCTGG ACCATTTAGA AGACGCCGGC AGGTAACTGG CCTCCCCAAA 000880
000881 CGCCCCGAAA ATTAAAAGCC TTAGGAGGCT TGTTCTGTGT TTGTGGTTTT GTAAAGGCAA TGCCCGCGGC AATAGGCCTG 000960
000961 GGAAAGTCGC ACTTTCATCC ACAAAGTTGA GGAGTTGCAA GGAATAATTG GGTGTCACAC CACAAGCAAC CTTGACTCGA 001040
001041 TCGGACCCCA CCCAGGATAC ACACAGACGC GCGCGCGCGC ACGCTTCCGA GTTTCCATTG AGAGTCTGGA AAGAGCATTT 001120
001121 CTTTCTTAAG TACCTGCGCT CAGCTAGAGC TCTCCCGGAG CATTTTAAAT ACTGAATGCC GAGCGGAGAA GGGAAACAGA 001200
001201 GTGTATTAAT CCCCACTCCG GTTGCCGGTG TCTGCAAGCC TCCTCTAAGC AGCGCAGGCG GCAGCCTGGA TGTCTGTGCG 001280
001281 CATCAAGGAG ACTTGCCGGC GCCAGAGTTG TGTCCACAGG TGCACTTGTG CCTCCCAAAG AGCGCGCGTA GAGACCATTT 001360
001361 CCCCTGCAAC GCCCCCCAGC CGAACACCCG CCGGGTGTGG CACCTCGGCC GAAACTCCTG GGGCGGCGCG GTGGAGCGTG 001440
001441 TGGAGGTTTC CGGGAAGACG CCTACGGCTG CGGCTCCGAC TGTGCGGGCT CCCGCCGCCC AGGCAAGAGC GTCCAGGAGC 001520
001521 GCGCTGGAAG CTGCGGCGCG CACCTTCCCC GGCGCAGTCT CTTGCCAGCC GGCGATCACG CAGAGCTGAA CCCCGCAGCT 001600
001601 AGGCGCGCAG GAAGGGCTGC ACAGAGTTTG AAGA