A novel role of NKX3.1 in the mitochondria regulating the transcription of the electron transport chain components is reported. Mechanistically, HSPA9 chaperones NKX3.1 into the mitochondria in response to oxidative stress to regulate reactive oxygen species and suppress tumor initiation..
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http://dx.doi.org/10.1158/2159-8290.CD-21-0861 | DOI Listing |
J Cell Biochem
February 2006
Department of Hematology and Oncology, Program in Genetics and Molecular Biology, Winship Cancer Institute, Emory University School of Medicine, 1365-C Clifton Road, Atlanta, GA 30322, USA.
Quantitative and structural genetic alterations cause the development and progression of prostate cancer. A number of genes have been implicated in prostate cancer by genetic alterations and functional consequences of the genetic alterations. These include the ELAC2 (HPC2), MSR1, and RNASEL (HPC1) genes that have germline mutations in familial prostate cancer; AR, ATBF1, EPHB2 (ERK), KLF6, mitochondria DNA, p53, PTEN, and RAS that have somatic mutations in sporadic prostate cancer; AR, BRCA1, BRCA2, CHEK2 (RAD53), CYP17, CYP1B1, CYP3A4, GSTM1, GSTP1, GSTT1, PON1, SRD5A2, and VDR that have germline genetic variants associated with either hereditary and/or sporadic prostate cancer; and ANXA7 (ANX7), KLF5, NKX3-1 (NKX3.
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