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Prostate cancer patients with low NKX3.1 expression are optimal candidates for intervention with 5alpha-reductase inhibitors as an adjunct to active surveillance.
During prostate cancer initiation, Nkx3.1 expression is frequently lost in both humans and mouse models. Data, including data from studies using cells from transgenic mice, suggest that androgens activate Nkx3.1 transcription via androgen receptor binding to 11-kb region in both normal luminal cells and castration-resistant prostatic neoplasm cells via androgen response elements in Nkx3.1 3prime untranslated region.
study demonstrated that expression of homeobox protein NK-3 homolog A(Nkx3.1) influenced both the timing and magnitude of the DNA damage response in the mouse prostate
Nkx3.1 loss and Tmprss2-ERG upregulation do not cooperate to enhance prostate tumorigenesis in vivo.
Id4 regulates NKX3.1, Sox9 and PTEN.
activated canonical Wnt signals and Nkx3.1 function in a positive feedback loop to regulate prostate bud growth and luminal epithelial differentiation.
multiple NKX3.1 binding sites were found in the RAMP1 locus in human prostate cancer cells and in the normal mouse prostate.
Deletions of Klf5 and Nkx3-1 do not have a additive effect in prostatic carcinogenesis in mouse model.
Transcriptional activation of prostate specific homeobox gene NKX3-1 in subsets of T-cell lymphoblastic leukemia (T-ALL).
Androgen-dependent transcription of the mouse Nkx3.1 gene is conferred through a noncanonical element within the intron of the gene.
Nkx3.1 has a role in bacterial prostatitis and its progression to inflammation and neoplasia
Data indicated that all cells expressing MYC in PIN lesions showed marked reductions in Nkx3.1, implicating MYC as a key factor that represses Nkx3.1 in PIN lesions.
Data show in Pten and Nkx3.1 mutant mice, cells with increased levels of SOX9 appeared within prostate epithelia at early stages of neoplasia, and higher expression correlated with progression at all stages of disease.
loss of function of Nkx3.1 and Pten cooperate in prostate carcinogeneis in mice.
Nkx3.1 mutant mice recapitulate early stages of prostate carcinogenesis.
Nkx3.1 contributes to the formation of the axial skeleton
Nkx3.1(+/-); Pten(+/-) mice recapitulate key features of advanced prostate cancer and represent a useful model for investigating associated molecular mechanisms and for evaluating therapeutic approaches.
Nkx3.1 homeobox gene has roles in prostate organogenesis and carcinogenesis (review)
Nkx3.1 and p27kip1 regulate prostatic epithelial cell proliferation and tumor initiation by affecting both haploinsufficient and nonhaploinsufficient pathways
Findings provide a molecular link between a gene whose inactivation is known to be involved in prostate carcinogenesis, namely Nkx3.1, and oxidative damage of the prostatic epithelium.
The tumour suppressors FOXP1 and NKX3.1, strongly implicated in PCa development, were identified as key transcription factors regulating TPbeta expression through Prm3 in both PCa cell lines.
NKX3.1 has potential utility as a prostate specific marker in the differential diagnostic distinction between nephrogenic adenoma and prostatic adenocarcinoma.
Low NKX3.1 expression is associated with hepatocellular carcinoma.
With deletion mutation analysis, plasmid construction, EMSA and oligonucleotide decoy technique, two Sp1-elements which located between +29 to +43 and -60 to -46 of NKX3.1 gene were identified and proven to be functional elements.
The androgen-regulated homeodomain transcription factor NKX3.1 plays roles in early prostate development and functions as a prostate-specific tumor suppressor.
the association between the down-regulation of PTEN and NKX3.1 genes contributed to prostate tumorigenesis.
NKX3.1 and DYRK1B were shown to interact via the DYRK1B kinase domain. In vitro kinase assay showed that DYRK1B phosphorylated NKX3.1 at serine 185, a residue critical for NKX3.1 steady-state turnover.
An NKX3.1 binding site polymorphism in the l-plastin promoter leads to differential gene expression in human prostate cancer
Analysis of prostate cancer tissues showed that the presence of a TMPRSS2-ERG rearrangement was highly correlated with lower levels of NKX3.1 expression consistent with the role of NKX3.1 as a suppressor of the pathogenic gene rearrangement.
NKX3.1 expression mediate beta-catenin and E-cadherin association and cell migration in prostate cells.
Our results indicate that variation in NKX3.1 expression combined with selenium or vitamin E treatment modifies the risk of prostate cancer.
NKX3.1 labelling is limited to estrogen/progesterone/androgen receptor-positive breast carcinomas.
These observations imply that the frequently noted loss-of-function of NKX3.1 cooperates with the activation of TMPRSS2-ERG fusions in prostate tumorigenesis.
NKX3.1 may enhance DNA integrity in prostate stem cells and may help to explain how cells differ in their sensitivity to DNA damage.
Androgens and NKX3.1 expression regulate the progression of the cell cycle and concurrently activate the DNA damage response.
Loci at 8q24 and 8q21 could influence susceptibility to prostate cancer in the northern Chinese population
This gene encodes a homeobox-containing transcription factor. This transcription factor functions as a negative regulator of epithelial cell growth in prostate tissue. Aberrant expression of this gene is associated with prostate tumor progression. Alternate splicing results in multiple transcript variants of this gene.
NK3 transcription factor related, locus 1
, NK3 homeobox 1
, Drosophila NK-3 transcription factor, locus 1
, homeobox protein NK-3 homolog A
, homeobox protein Nkx-3.1
, NK homeobox, family 3, A
, NK3 transcription factor homolog A
, NK-3 transcription factor, locus 1