scholarly journals RNA splicing and splicing regulator changes in prostate cancer pathology

2017 ◽  
Vol 136 (9) ◽  
pp. 1143-1154 ◽  
Author(s):  
Jennifer Munkley ◽  
Karen Livermore ◽  
Prabhakar Rajan ◽  
David J. Elliott
Keyword(s):  
Prostate Cancer ◽  
Rna Splicing ◽  
Cancer Pathology ◽  
Splicing Regulator

Molecular prostate cancer pathology: Current issues and achievements

2005 ◽  
Vol 39 (sup216) ◽  
pp. 82-93 ◽  
Author(s):  
Jack A. Schalken ◽  
Anders Bergh ◽  
Aldo Bono ◽  
Christopher Foster ◽  
Mary Gospadarowicz ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Pathology

scholarly journals Preclinical studies using cisplatin/carboplatin to restore the Enzalutamide sensitivity via degrading the androgen receptor splicing variant 7 (ARv7) to further suppress Enzalutamide resistant prostate cancer

2020 ◽  
Vol 11 (11) ◽  
Author(s):  
Fu-Ju Chou ◽  
ChangYi Lin ◽  
Hao Tian ◽  
WanYing Lin ◽  
Bosen You ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Androgen Receptor ◽  
Rna Splicing ◽  
Preclinical Studies ◽  
Castration Resistant Prostate Cancer ◽  
Splicing Variant ◽  
Castration Resistant ◽  
Lncrna Malat1 ◽  
Near Future

Abstract The FDA-approved anti-androgen Enzalutamide (Enz) has been used successfully as the last line therapy to extend castration-resistant prostate cancer (CRPC) patients’ survival by an extra 4.8 months. However, CRPC patients eventually develop Enz-resistance that may involve the induction of the androgen receptor (AR) splicing variant ARv7. Here we found that Cisplatin (Cis) or Carboplatin, currently used in chemotherapy/radiation therapy to suppress tumor progression, could restore the Enz sensitivity in multiple Enz-resistant (EnzR) CRPC cells via directly degrading/suppressing the ARv7. Combining Cis or Carboplatin with Enz therapy can also delay the development of Enz-resistance in CRPC C4-2 cells. Mechanism dissection found that Cis or Carboplatin might decrease the ARv7 expression via multiple mechanisms including targeting the lncRNA-Malat1/SF2 RNA splicing complex and increasing ARv7 degradation via altering ubiquitination. Preclinical studies using in vivo mouse model with implanted EnzR1-C4-2 cells also demonstrated that Cis plus Enz therapy resulted in better suppression of EnzR CRPC progression than Enz treatment alone. These results not only unveil the previously unrecognized Cis mechanism to degrade ARv7 via targeting the Malat1/SF2 complex and ubiquitination signals, it may also provide a novel and ready therapy to further suppress the EnzR CRPC progression in the near future.

scholarly journals Multiple Tissue Biomarkers Independently and Additively Predict Prostate Cancer Pathology Outcomes

2021 ◽  
Vol 79 (1) ◽  
pp. 141-149
Author(s):  
Matthew R. Cooperberg ◽  
Janet E. Cowan ◽  
Karla J. Lindquist ◽  
Yasuko Kobayashi ◽  
Jeffry P. Simko ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Pathology ◽  
Tissue Biomarkers

scholarly journals RNA Splicing of the BHC80 Gene Contributes to Neuroendocrine Prostate Cancer Progression

2019 ◽  
Vol 76 (2) ◽  
pp. 157-166 ◽  
Author(s):  
Yinan Li ◽  
Ning Xie ◽  
Ruiqi Chen ◽  
Ahn R. Lee ◽  
Jessica Lovnicki ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Progression ◽  
Rna Splicing ◽  
Prostate Cancer Progression ◽  
Neuroendocrine Prostate Cancer

scholarly journals MP04-07 POVERTY IS ASSOCIATED WITH ADVERSE PROSTATE CANCER PATHOLOGY AMONG AFRICAN-AMERICAN MEN UNDERGOING RADICAL PROSTATECTOMY

2016 ◽  
Vol 195 (4S) ◽  
Author(s):  
Samuel Weprin ◽  
Joshua Jones ◽  
Joshua Kaplan ◽  
Andrew Harbin ◽  
Anastasiya Kamenko ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
African American ◽  
Radical Prostatectomy ◽  
African American Men ◽  
Cancer Pathology

RNA‐Binding Protein QKI is a critical pre‐RNA splicing regulator for cardiac development and function

2020 ◽  
Vol 34 (S1) ◽  
pp. 1-1
Author(s):  
Ying Liu ◽  
Xinyun Chen ◽  
Chen Xu ◽  
Ning Sun ◽  
Weinian Shou
Keyword(s):  
Rna Splicing ◽  
Rna Binding ◽  
Cardiac Development ◽  
Binding Protein ◽  
Rna Binding Protein ◽  
Splicing Regulator ◽  
And Function

scholarly journals How does Tra2β protein regulate tissue-specific RNA splicing?

2012 ◽  
Vol 40 (4) ◽  
pp. 784-788 ◽  
Author(s):  
David J. Elliott ◽  
Andrew Best ◽  
Caroline Dalgliesh ◽  
Ingrid Ehrmann ◽  
Sushma Grellscheid
Keyword(s):  
Rna Splicing ◽  
Mouse Development ◽  
Tissue Specific ◽  
Rna Targets ◽  
Regulator Protein ◽  
Mouse Tissues ◽  
Splicing Regulator ◽  
Alternatively Spliced ◽  
High Concentrations

The splicing regulator protein Tra2β is conserved between humans and insects and is essential for mouse development. Recent identification of physiological RNA targets has started to uncover molecular targets and mechanisms of action of Tra2β. At a transcriptome-wide level, Tra2β protein binds a matrix of AGAA-rich sequences mapping frequently to exons. Particular tissue-specific alternatively spliced exons contain high concentrations of high scoring Tra2β-binding sites and bind Tra2β strongly in vitro. These top exons were also activated for splicing inclusion in cellulo by co-expression of Tra2β protein and were significantly down-regulated after genetic depletion of Tra2β. Tra2β itself seems to be fairly evenly expressed across several different mouse tissues. In the present paper, we review the properties of Tra2β and its regulated target exons, and mechanisms through which this fairly evenly expressed alternative splicing regulator might drive tissue-specific splicing patterns.

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