Difference between revisions of "LNCSRLR"

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(Created page with "==Annotated Information== ===Approved Symbol=== LNCSRLR ===Approved Name=== lncRNA sorafenib resistance in renal cell carcinoma associated ===Previous Symbols=== _ ===Synonyms...")
 
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==Annotated Information==
 
==Annotated Information==
===Approved Symbol===
+
===Name===
LNCSRLR
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LNCSRLR:lncRNA sorafenib resistance in renal cell carcinoma associated
===Approved Name===
+
 
lncRNA sorafenib resistance in renal cell carcinoma associated
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lncRNA-SRLR<ref name="ref1" />
===Previous Symbols===
+
===Characteristics===
_
+
LncRNA-SRLR is located on chromosome 3 in humans and is composed of 2 exons with a poly (A) tail and has a full length of 663 nt, as determined via a rapid amplification of cDNA ends assay.<ref name="ref1" />
===Synonyms===
+
 
lncRNA-SRLR
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===Cellular Localization===
===Chromosome===
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The subcellular distribution assay reveals that lncRNA-SRLR is predominately located in the nucleus.<ref name="ref1" />
3q24
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===RefSeq ID===
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===Function===
_
+
[[
===OMIM ID===
+
LncRNA-SRLR knockdown sensitizes nonresponsive RCC cells to sorafenib treatment, whereas the overexpression of lncRNA-SRLR confers sorafenib resistance to responsive RCC cells. Mechanistically, lncRNA-SRLR directly binds to NF-κB and promotes IL-6 transcription, leading to the activation of STAT3 and the development of sorafenib tolerance. A STAT3 inhibitor and IL-6-receptor antagonist both restore the response to sorafenib treatment. Moreover, a clinical investigation demonstrates that high levels of lncRNA-SRLR correlates with poor responses to sorafenib therapy in RCC patients.<ref name="ref1" />
_
+
 
===RefSeq(supplied by NCBI)===
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===Expression===
_
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LncRNA-SRLR is preferentially upregulated in RCCs(Renal cell carcinoma) with inherent sorafenib resistance.<ref name="ref1" />
===pubmed IDs===
+
===Diseases===
27841868
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Renal cell carcinoma<ref name="ref1" />
 +
==Labs working on this lncRNA==
 +
*Department of Urology, Changzheng Hospital, Second Military Medical University, Shanghai, China.
 +
==References==
 +
<references>
 +
<ref name="ref1">
 +
Xu Z, Yang F, Wei D, Liu B, Chen C, Bao Y, Wu Z, Wu D, Tan H, Li J, Wang J,
 +
Liu J, Sun S, Qu L, Wang L. Long noncoding RNA-SRLR elicits intrinsic sorafenib
 +
resistance via evoking IL-6/STAT3 axis in renal cell carcinoma. Oncogene. 2017
 +
Apr 6;36(14):1965-1977.
 +
</ref>
 +
</references>

Revision as of 06:55, 7 November 2017

Annotated Information

Name

LNCSRLR:lncRNA sorafenib resistance in renal cell carcinoma associated

lncRNA-SRLR[1]

Characteristics

LncRNA-SRLR is located on chromosome 3 in humans and is composed of 2 exons with a poly (A) tail and has a full length of 663 nt, as determined via a rapid amplification of cDNA ends assay.[1]

Cellular Localization

The subcellular distribution assay reveals that lncRNA-SRLR is predominately located in the nucleus.[1]

Function

[[ LncRNA-SRLR knockdown sensitizes nonresponsive RCC cells to sorafenib treatment, whereas the overexpression of lncRNA-SRLR confers sorafenib resistance to responsive RCC cells. Mechanistically, lncRNA-SRLR directly binds to NF-κB and promotes IL-6 transcription, leading to the activation of STAT3 and the development of sorafenib tolerance. A STAT3 inhibitor and IL-6-receptor antagonist both restore the response to sorafenib treatment. Moreover, a clinical investigation demonstrates that high levels of lncRNA-SRLR correlates with poor responses to sorafenib therapy in RCC patients.[1]

Expression

LncRNA-SRLR is preferentially upregulated in RCCs(Renal cell carcinoma) with inherent sorafenib resistance.[1]

Diseases

Renal cell carcinoma[1]

Labs working on this lncRNA

  • Department of Urology, Changzheng Hospital, Second Military Medical University, Shanghai, China.

References

  1. 1.0 1.1 1.2 1.3 1.4 1.5 Xu Z, Yang F, Wei D, Liu B, Chen C, Bao Y, Wu Z, Wu D, Tan H, Li J, Wang J, Liu J, Sun S, Qu L, Wang L. Long noncoding RNA-SRLR elicits intrinsic sorafenib resistance via evoking IL-6/STAT3 axis in renal cell carcinoma. Oncogene. 2017 Apr 6;36(14):1965-1977.