Significance of capsular attachment and invasion of cancer tissues in prostate cancer

2003 ◽  
Vol 10 (6) ◽  
pp. 309-314 ◽  
Author(s):  
MASASHI TANAKA ◽  
NORIYUKI SUZUKI ◽  
HIROOMI NAKATSU ◽  
SHINO MURAKAMI ◽  
OSAMU MATSUZAKI ◽  
...  
2017 ◽  
Vol 12 (1) ◽  
Author(s):  
Melissa A. Yow ◽  
◽  
Sepehr N. Tabrizi ◽  
Gianluca Severi ◽  
Damien M. Bolton ◽  
...  

2005 ◽  
Vol 206 (2) ◽  
pp. 214-219 ◽  
Author(s):  
Tine Van de Sande ◽  
Tania Roskams ◽  
Evelyne Lerut ◽  
Steven Joniau ◽  
Hein Van Poppel ◽  
...  

Cancers ◽  
2020 ◽  
Vol 12 (7) ◽  
pp. 1814 ◽  
Author(s):  
Andras Franko ◽  
Yaping Shao ◽  
Martin Heni ◽  
Jörg Hennenlotter ◽  
Miriam Hoene ◽  
...  

Despite it being the most common incident of cancer among men, the pathophysiological mechanisms contributing to prostate cancer (PCa) are still poorly understood. Altered mitochondrial metabolism is postulated to play a role in the development of PCa. To determine the key metabolites (which included mitochondrial oncometabolites), benign prostatic and cancer tissues of patients with PCa were analyzed using capillary electrophoresis and liquid chromatography coupled with mass spectrometry. Gene expression was studied using real-time PCR. In PCa tissues, we found reduced levels of early tricarboxylic acid cycle metabolites, whereas the contents of urea cycle metabolites including aspartate, argininosuccinate, arginine, proline, and the oncometabolite fumarate were higher than that in benign controls. Fumarate content correlated positively with the gene expression of oncogenic HIF1α and NFκB pathways, which were significantly higher in the PCa samples than in the benign controls. Furthermore, data from the TCGA database demonstrated that prostate cancer patients with activated NFκB pathway had a lower survival rate. In summary, our data showed that fumarate content was positively associated with carcinogenic genes.


2008 ◽  
Vol 82 (20) ◽  
pp. 9964-9977 ◽  
Author(s):  
Sanggu Kim ◽  
Namshin Kim ◽  
Beihua Dong ◽  
David Boren ◽  
Serena A. Lee ◽  
...  

ABSTRACT Xenotropic murine leukemia virus-related virus (XMRV) is a new human gammaretrovirus identified in prostate cancer tissue from patients homozygous for a reduced-activity variant of the antiviral enzyme RNase L. Neither a casual relationship between XMRV infection and prostate cancer nor a mechanism of tumorigenesis has been established. To determine the integration site preferences of XMRV and the potential risk of proviral insertional mutagenesis, we carried out a genome-wide analysis of viral integration sites in the prostate cell line DU145 after an acute XMRV infection and compared the integration site pattern of XMRV with those found for murine leukemia virus and two human retroviruses, human immunodeficiency virus type 1 and human T-cell leukemia virus type 1. Among all retroviruses analyzed, XMRV has the strongest preference for transcription start sites, CpG islands, DNase-hypersensitive sites, and gene-dense regions; all are features frequently associated with structurally open transcription regulatory regions of a chromosome. Analyses of XMRV integration sites in tissues from prostate cancer patients found a similar preference for the aforementioned chromosomal features. Additionally, XMRV integration sites in cancer tissues were associated with cancer breakpoints, common fragile sites, microRNA, and cancer-related genes, suggesting a selection process that favors certain chromosomal integration sites. In both acutely infected cells and cancer tissues, no common integration site was detected within or near proto-oncogenes or tumor suppressor genes. These results are consistent with a model in which XMRV may contribute to tumorigenicity via a paracrine mechanism.


2018 ◽  
Vol 13 (1) ◽  
pp. 511-517 ◽  
Author(s):  
Bin Li ◽  
Zhe Lin ◽  
Quan Liang ◽  
Yuan Hu ◽  
Wen-Feng Xu

AbstractObjectiveThis study aimed to evaluate the expression of progestin and adipoQ receptor family member VI (PAQR6, mPRδ) in prostate cancer and to explore its role in prostate cancer progression.MethodsPAQR6 mRNA expression was evaluated based on the data obtained from the TCGA database and the GEO database. The prognostic value of PAQR6 was explored by Kaplan-Meier analysis. To investigate the role of PAQR6, it was depleted by siRNA in DU145 cells. The effects of depleting PAQR6 on DU145 cell viability and migration were determined by CCK8 assay, colony formation assay, and wound healing assay, respectively. The activation of MEK and ERK were analyzed by western blot.ResultsPAQR6 mRNA expression was significantly up-regulated in prostate cancer tissues and correlated with lower survival rates (p=0.014). Furthermore, qPCR revealed that PAQR6 expression was elevated in DU145 and LNCaP cells compared with RWPE-2 cells. Depleting PAQR6 obviously suppressed DU145 cell proliferation and migration (p<0.01). In addition, the ratio of p-MEK/MEK and p-ERK/ERK was significantly reduced after silencing PAQR6 (p<0.01).ConclusionPAQR6 might play a facilitating role in prostate cancer development by regulating the MAPK signaling pathway. Moreover, it might serve as a potential predictor and therapeutic target in prostate cancer.


2010 ◽  
Vol 391 (4) ◽  
Author(s):  
Astrid K. Whitbread ◽  
Tara L. Veveris-Lowe ◽  
Ying Dong ◽  
Olivia L. Tan ◽  
Robert Gardiner ◽  
...  

Abstract PSA-RP2 is a variant transcript expressed from the PSA gene that is conserved in gorillas, chimpanzees and humans suggesting a particular relevance for this transcript in these primates. We demonstrated by qRT-PCR that PSA-RP2 is upregulated in prostate cancer compared with benign prostatic hyperplasia tissues. The PSA-RP2 protein was not detected in seminal fluid and was cytoplasmically localised but not secreted from LNCaP or transfected PC3 prostate cells, despite secretion from transfected Cos-7 and HEK293 kidney cell lines. PSA-RP2-transfected PC3 cells showed slightly decreased proliferation and increased migration towards PC3-conditioned medium that could suggest a functional role in prostate cancer.


Epigenetics ◽  
2015 ◽  
Vol 10 (4) ◽  
pp. 319-328 ◽  
Author(s):  
JM Devaney ◽  
S Wang ◽  
P Furbert-Harris ◽  
V Apprey ◽  
M Ittmann ◽  
...  

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