LncRNA SARCC is differentially regulated by hypoxia in a von Hippel-Lindau (VHL)-dependent manner both in renal cell carcinoma (RCC) cell culture and clinical specimens. SARCC can suppress hypoxic cell cycle progression in the VHL-mutant RCC cells while derepress it in the VHL-restored RCC cells. Mechanism dissection reveals that SARCC can post-transcriptionally regulate androgen receptor (AR) by physically binding and destablizing AR protein to suppress AR/HIF-2α/C-MYC signals. In return, HIF-2α can transcriptionally regulate the SARCC expression via binding to hypoxia-responsive elements on the promoter of SARCC. The negative feedback modulation between SARCC/AR complex and HIF-2α signaling may then lead to differentially modulated RCC progression in a VHL-dependent manner (1).
|LncRNA||tissue||cancer type||expression level||oncogene/suppress gene||pathway||binding gene/factor||associated gene/factor||proliferation||apoptosis||migration||EMT||invasion||metastasis||prognosis||tag||PMID|
. Zhai W, Sun Y, Jiang M, Wang M, Gasiewicz TA, et al. (2016). Differential regulation of LncRNA-SARCC suppresses VHL-mutant RCC cell proliferation yet promotes VHL-normal RCC cell proliferation via modulating androgen receptor/HIF-2α/C-MYC axis under hypoxia. Oncogene 35(37): 4866-80. link pubmed