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Annotated Information


LNCSRLR:lncRNA sorafenib resistance in renal cell carcinoma associated



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]


Schematic diagram of lncRNA-SRLR-based regulatory mechanism in RCC cells[1].

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 of LNCSRLR[1].

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


Renal cell carcinoma[1]

Labs working on this lncRNA

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


  1. 1.0 1.1 1.2 1.3 1.4 1.5 1.6 1.7 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.