CHC1-L, a candidate gene for prostate carcinogenesis at 13q14.2, is frequently affected by loss of heterozygosity and underexpressed in human prostate cancer

2002 ◽  
Vol 99 (5) ◽  
pp. 689-696 ◽  
Author(s):  
Alain Latil ◽  
Patrice Morant ◽  
Georges Fournier ◽  
Philippe Mangin ◽  
Philippe Berthon ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Candidate Gene ◽  
Loss Of Heterozygosity ◽  
Human Prostate ◽  
Human Prostate Cancer ◽  
Prostate Carcinogenesis

Loss of heterozygosity at chromosome arm 13q and RB1 status in human prostate cancer

1999 ◽  
Vol 30 (7) ◽  
pp. 809-815 ◽  
Author(s):  
Alain Latil ◽  
Ivan Bièche ◽  
Sandrine Pesche ◽  
Alain Volant ◽  
Antoine Valèri ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Loss Of Heterozygosity ◽  
Human Prostate ◽  
Human Prostate Cancer ◽  
Chromosome Arm

scholarly journals BRF1 accelerates prostate tumourigenesis and perturbs immune infiltration

Oncogene ◽  
2019 ◽  
Vol 39 (8) ◽  
pp. 1797-1806 ◽  
Author(s):  
Carolyn J. Loveridge ◽  
Sarah Slater ◽  
Kirsteen J. Campbell ◽  
Noor A. Nam ◽  
John Knight ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Rna Polymerase Iii ◽  
Adaptive Immune Response ◽  
Human Prostate ◽  
Limiting Factor ◽  
Complement Factor ◽  
Human Prostate Cancer ◽  
Prostate Carcinogenesis ◽  
Immune Pathway

AbstractBRF1 is a rate-limiting factor for RNA Polymerase III-mediated transcription and is elevated in numerous cancers. Here, we report that elevated levels of BRF1 associate with poor prognosis in human prostate cancer. In vitro studies in human prostate cancer cell lines demonstrated that transient overexpression of BRF1 increased cell proliferation whereas the transient downregulation of BRF1 reduced proliferation and mediated cell cycle arrest. Consistent with our clinical observations, BRF1 overexpression in a Pten-deficient mouse (PtenΔ/ΔBRF1Tg) prostate cancer model accelerated prostate carcinogenesis and shortened survival. In PtenΔ/ΔBRF1Tg tumours, immune and inflammatory processes were altered, with reduced tumoral infiltration of neutrophils and CD4 positive T cells, which can be explained by decreased levels of complement factor D (CFD) and C7 components of the complement cascade, an innate immune pathway that influences the adaptive immune response. We tested if the secretome was involved in BRF1-driven tumorigenesis. Unbiased proteomic analysis on BRF1-overexpresing PC3 cells confirmed reduced levels of CFD in the secretome, implicating the complement system in prostate carcinogenesis. We further identify that expression of C7 significantly correlates with expression of CD4 and has the potential to alter clinical outcome in human prostate cancer, where low levels of C7 associate with poorer prognosis.

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