Clinical and Functional Analyses of p73R1 Mutations in Prostate Cancer

2005 ◽  
Author(s):  
Wanguo Liu
2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Ray-Chang Wu ◽  
In-Chi Young ◽  
Yu-Fang Chen ◽  
Sung-Ting Chuang ◽  
Antoun Toubaji ◽  
...  

Abstract PTEN is frequently mutated in prostate cancer. The tumor suppressor function of PTEN is attributed to its lipid phosphatase activity that counters PI3K action. Here, we report a PTEN-ARID4B-PI3K axis in which PTEN inhibits expression of ARID4B, while ARID4B is a transcriptional activator of the PI3K subunit genes PIK3CA and PIK3R2 that are crucial for activation of the PI3K/AKT pathway. Reciprocal binding of ARID4B and histone H1 to the PIK3CA and PIK3R2 promoters modulates chromatin condensation, suggesting a mechanism by which ARID4B activates these promoters. Functional analyses reveals that ARID4B is required for prostate tumorigenesis when PTEN is deficient. The biological significance is further substantiated by the existence of a PTEN/ARID4B/PIK3CA three-gene signature that improves the predictive power for prostate cancer recurrence in patients. In summary, we identify ARID4B as a master regulator in the PTEN-PI3K pathway, thus providing a potential therapeutic target for prostate cancer carrying PTEN mutations.


2012 ◽  
Vol 109 (28) ◽  
pp. 11252-11257 ◽  
Author(s):  
C. Grisanzio ◽  
L. Werner ◽  
D. Takeda ◽  
B. C. Awoyemi ◽  
M. M. Pomerantz ◽  
...  

2014 ◽  
Vol 395 (11) ◽  
pp. 1275-1290 ◽  
Author(s):  
Melanie Weiss ◽  
Christoph Plass ◽  
Clarissa Gerhauser

Abstract Prostate cancer (PCa) is the second most common cause of cancer-related deaths in men. Despite advances in the characterization of genomic and epigenetic aberrations contributing to PCa, the etiology of PCa is still far from being understood. Research over the past decade demonstrated the role of long non-coding RNAs (lncRNAs) in deregulation of target genes mainly through epigenetic mechanisms. In PCa, evidence accumulated that hundreds of lncRNAs are dysregulated. Functional analyses revealed their contribution to prostate carcinogenesis by targeting relevant pathways and gene regulation mechanisms including PTEN/AKT and androgen receptor signaling as well as chromatin remodeling complexes. Here we summarize our current knowledge on the roles of lncRNAs in PCa and their potential use as biomarkers for aggressive PCa and as novel therapeutic targets.


2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Zengshu Xing ◽  
Sailian Li ◽  
Zhenxiang Liu ◽  
Chong Zhang ◽  
Zhiming Bai

Abstract Background Prostate cancer (PCa) belongs to an epithelial malignancy that occurs in the prostate gland and is the most common malignancy of the male genitourinary system. Referring to related literature, circSERPINA3 has been reported to be up-regulated in PCa. However, its biological function remains unclear. Purpose This study aimed to reveal the specific role and relevant molecular mechanism of circSERPINA3 in PCa. Methods RT-qPCR was used to examine gene expression and functional analyses were conducted to verify the effect of circSERPINA3 on cell apoptosis, autophagy and aerobic glycolysis in PCa cells. Mechanism assays were applied to evaluate the relationship among circSERPINA3/miR-653-5p/SERPINA3/BUD13. Results CircSERPINA3 was verified to be up-regulated in PCa cells and to inhibit cell apoptosis while promoting aerobic glycolysis and autophagy in PCa cells. CircSERPINA3 and SERPINA3 were also testified to bind to miR-653-5p through a line of mechanism experiments. Moreover, it was discovered that circSERPINA3 could stabilize SERPINA3 mRNA via recruiting BUD13. Additionally, SERPINA3 was verified to inhibit cell apoptosis, while promoting aerobic glycolysis and autophagy in PCa cells. Conclusions Our study suggested that circSERPINA3 regulated apoptosis, autophagy and aerobic glycolysis of PCa cells by competitively binding to miR-653-5p and recruiting BUD13. Graphic abstract


2020 ◽  
Author(s):  
Kaiyu Qian ◽  
Gang Wang ◽  
Lingao Ju ◽  
Jiyan Liu ◽  
Hang Zheng ◽  
...  

Abstract5-10% of total prostate cancer (PCa) cases are hereditary. Particularly, immunocheckpoint inhibitor-sensitive tandem duplicator phenotype (TDP) accounts for 6.9% PCa cases, whereas genetic susceptibility genes remain completely unknown. We identified a Chinese family with two PCa patients, in which the PCa phenotype co-segregated with a rare germline variant EGFRR831H. Patient-derived conditionally reprogrammed cells (CRC) exhibited increased EGFR and AKT phosphorylation, and a sensitivity to EGFR antagonist Afatinib in migration assays, suggesting the EGFR allele was constitutively active. Both EGFRR831H-mutant tumors contained biallelic CDK12 inactivation, together with prominent tandem duplication across the genome. These somatic mutations could be detected in urine before surgery. Analysis of public databases showed a significant correlation between mutation status of EGFR and CDK12. Taken together, our genetic and functional analyses identified a previously undescribed link between EGFR and prostate cancer.


2008 ◽  
Vol 22 (S1) ◽  
Author(s):  
Kazuo Koike ◽  
Kazutake Tsujikawa ◽  
Kaori Kitae ◽  
Hiroshi Arima ◽  
Takashi Suzuki ◽  
...  

2001 ◽  
Vol 120 (5) ◽  
pp. A284-A284
Author(s):  
T BOLIN ◽  
A KNEEBONE ◽  
T LARSSON
Keyword(s):  

2007 ◽  
Vol 177 (4S) ◽  
pp. 538-539
Author(s):  
Joseph F. Pazona ◽  
C. Shad Thaxton ◽  
Neema Navai ◽  
Brian T. Helfand ◽  
Lee C. Zhao ◽  
...  
Keyword(s):  

2007 ◽  
Vol 177 (4S) ◽  
pp. 77-78
Author(s):  
Christopher R. Porter ◽  
Jochen Walz ◽  
Andrea Gallina ◽  
Claudio Jeldres ◽  
Koichi Kodama ◽  
...  

2007 ◽  
Vol 177 (4S) ◽  
pp. 156-156
Author(s):  
Andrea Salonia ◽  
Pierre I. Karakiewicz ◽  
Andrea Gallina ◽  
Alberto Briganti ◽  
Tommaso C. Camerata ◽  
...  

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