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The  ESRRA  gene encodes a transcription factor and regulates several genes, such as  WNT11  and  OPN , involved in tumorigenesis. It is upregulated in several cancers, including OSCC. We have previously shown that the tumor suppressor miR-125a targets  ESRRA , and its downregulation causes upregulation of ESRRA in OSCC. Upregulation of ESRRA in the absence of downregulation of miR-125a in a subset of OSCC samples suggests the involvement of an alternative mechanism. Using TaqMan ®  copy number assay, here we report for the first time that the genomic amplification of  ESRRA  causes its upregulation in a subset of OSCC samples. Ectopic overexpression of ESRRA led to accelerated cell proliferation, anchorage-independent cell growth and invasion, and inhibited apoptosis. Whereas, knockdown of ESRRA expression by siRNA led to reduced cell proliferation, anchorage-independent cell growth and invasion, and accelerated apoptosis. Furthermore, the delivery of a synthetic biostable  ESRRA  siRNA to OSCC cells resulted in regression of xenografts in nude mice. Thus, the genomic amplification of  ESRRA  is another novel mechanism for its upregulation in OSCC. Based on our  in vitro  and  in vivo  experiments, we suggest that targeting  ESRRA  by siRNA could be a novel therapeutic strategy for OSCC and other cancers.

Genomic amplification upregulates estrogen-related receptor alpha and its depletion inhibits oral squamous cell carcinoma tumors in vivo