scholarly journals Identification of RNA-binding protein SNRPA1 for prognosis in prostate cancer

Aging ◽  
2021 ◽  
Author(s):  
Penghui Yuan ◽  
Le Ling ◽  
Xintao Gao ◽  
Taotao Sun ◽  
Jianping Miao ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Rna Binding ◽  
Binding Protein ◽  
Rna Binding Protein

INVESTIGATION OF THE ROLE OF GRSF-1 RNA BINDING PROTEIN IN PROSTATE CANCER PROGRESSION

1999 ◽  
pp. 61
Author(s):  
Michael E. Chen ◽  
Gail C. Fraizer ◽  
Tasneem Ahmed ◽  
Bei Zheng ◽  
Jeffrey Wilusz ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Progression ◽  
Rna Binding ◽  
Binding Protein ◽  
Rna Binding Protein ◽  
Prostate Cancer Progression

scholarly journals LncRNA SNHG1 and RNA Binding Protein hnRNPL form a Complex and Coregulate CDH1 to Boost the Growth and Metastasis of Prostate Cancer

2020 ◽  
Author(s):  
Xiao Tan ◽  
Wen-Bin Chen ◽  
Dao-Jun Lv ◽  
Tao-Wei Yang ◽  
Kai-Hui Wu ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Rna Binding ◽  
Epithelial Mesenchymal Transition ◽  
Binding Protein ◽  
Expression Profiles ◽  
Mrna Level ◽  
Rna Binding Protein ◽  
Loss Of Function ◽  
Mesenchymal Transition ◽  
E Cadherin

Abstract Background: The interaction between LncRNA and RNA-binding protein (RBPs) plays an essential role in the regulation over the malignant progression of tumors. Previous studies on the mechanism of SNHG1, an emerging lncRNA, have primarily focused on the competing endogenous RNA (ceRNA) mechanism. Nevertheless, the underlying mechanism between SNHG1 and RBPs in tumors remains to be explored, especially in prostate cancer (PCa).Methods：SNHG1 expression profiles in PCa were determined through the analysis of TCGA data and tissue microarray at the mRNA level. Gain- and loss-of-function experiments were performed to investigate the biological role of SNHG1 in PCa initiation and progression. RNA-seq, immunoblotting, RNA pull-down and RNA immunoprecipitation analyses were utilized to clarify potential pathways with which SNHG1 might be involved. Finally, rescue experiments were carried out to further confirm this mechanism.Results: We found that SNHG1 was dominantly expressed in the nuclei of PCa cells and significantly upregulated in PCa patients. The higher expression level of SNHG1 was dramatically correlated with tumor metastasis and patient survival. Functionally, overexpression of SNHG1 in PCa cells induced epithelial–mesenchymal transition (EMT), accompanied by down-regulation of the epithelial marker, E-cadherin, and up-regulation of the mesenchymal marker, vimentin. Increased proliferation and migration, as well as accelerated xenograft tumor growth, were observed in SNHG1-overexpressing PCa cells, while opposite effects were achieved in SNHG1-silenced cells. Mechanistically, SNHG1 competitively interacted with hnRNPL to impair the translation of protein E-cadherin, thus activating the effect of SNHG1 on the EMT pathway, eventually promoting the metastasis of PCa. Conclusion: Our findings demonstrate that SNHG1 is a positive regulator of EMT activation through the SNHG1-hnRNPL-CDH1 axis. SNHG1 may serve as a novel potential therapeutic target for PCa.

scholarly journals RNA‐binding protein Musashi2 stabilizing androgen receptor drives prostate cancer progression

2020 ◽  
Vol 111 (2) ◽  
pp. 369-382
Author(s):  
Jing Zhao ◽  
Yu Zhang ◽  
Xi‐sheng Liu ◽  
Fang‐ming Zhu ◽  
Feng Xie ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Androgen Receptor ◽  
Cancer Progression ◽  
Rna Binding ◽  
Binding Protein ◽  
Rna Binding Protein ◽  
Prostate Cancer Progression

scholarly journals The RNA-binding protein hnRNPA2 regulates β-catenin protein expression and is overexpressed in prostate cancer

RNA Biology ◽  
2014 ◽  
Vol 11 (6) ◽  
pp. 755-765 ◽  
Author(s):  
Jacqueline Stockley ◽  
M Eugenia M Villasevil ◽  
Colin Nixon ◽  
Imran Ahmad ◽  
Hing Y Leung ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Protein Expression ◽  
Rna Binding ◽  
Binding Protein ◽  
Rna Binding Protein

scholarly journals LncRNA SNHG1 and RNA binding protein hnRNPL form a complex and coregulate CDH1 to boost the growth and metastasis of prostate cancer

2021 ◽  
Vol 12 (2) ◽  
Author(s):  
Xiao Tan ◽  
Wen-bin Chen ◽  
Dao-jun Lv ◽  
Tao-wei Yang ◽  
Kai-hui Wu ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Rna Binding ◽  
Epithelial Mesenchymal Transition ◽  
Binding Protein ◽  
Expression Profiles ◽  
Rna Binding Protein ◽  
Underlying Mechanism ◽  
Loss Of Function ◽  
Mesenchymal Transition ◽  
E Cadherin

AbstractThe interaction between LncRNA and RNA-binding protein (RBPs) plays an essential role in the regulation over the malignant progression of tumors. Previous studies on the mechanism of SNHG1, an emerging lncRNA, have primarily focused on the competing endogenous RNA (ceRNA) mechanism. Nevertheless, the underlying mechanism between SNHG1 and RBPs in tumors remains to be explored, especially in prostate cancer (PCa). SNHG1 expression profiles in PCa were determined through the analysis of TCGA data and tissue microarray at the RNA level. Gain- and loss-of-function experiments were performed to investigate the biological role of SNHG1 in PCa initiation and progression. RNA-seq, immunoblotting, RNA pull-down and RNA immunoprecipitation analyses were utilized to clarify potential pathways with which SNHG1 might be involved. Finally, rescue experiments were carried out to further confirm this mechanism. We found that SNHG1 was dominantly expressed in the nuclei of PCa cells and significantly upregulated in PCa patients. The higher expression level of SNHG1 was dramatically correlated with tumor metastasis and patient survival. Functionally, overexpression of SNHG1 in PCa cells induced epithelial–mesenchymal transition (EMT), accompanied by down-regulation of the epithelial marker, E-cadherin, and up-regulation of the mesenchymal marker, vimentin. Increased proliferation and migration, as well as accelerated xenograft tumor growth, were observed in SNHG1-overexpressing PCa cells, while opposite effects were achieved in SNHG1-silenced cells. Mechanistically, SNHG1 competitively interacted with hnRNPL to impair the translation of protein E-cadherin, thus activating the effect of SNHG1 on the EMT pathway, eventually promoting the metastasis of PCa. Our findings demonstrate that SNHG1 is a positive regulator of EMT activation through the SNHG1-hnRNPL-CDH1 axis. SNHG1 may serve as a novel potential therapeutic target for PCa.

scholarly journals Dysregulation of spliceosome gene expression in advanced prostate cancer by RNA-binding protein PSF

2017 ◽  
Vol 114 (39) ◽  
pp. 10461-10466 ◽  
Author(s):  
Ken-ichi Takayama ◽  
Takashi Suzuki ◽  
Tetsuya Fujimura ◽  
Yuta Yamada ◽  
Satoru Takahashi ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
High Speed ◽  
Rna Binding ◽  
Binding Protein ◽  
Rna Binding Protein ◽  
Hormone Refractory Prostate Cancer ◽  
Therapeutic Approaches ◽  
Gene Expressions ◽  
Therapeutic Possibility ◽  
Hormone Refractory

Developing therapeutic approaches are necessary for treating hormone-refractory prostate cancer. Activation of androgen receptor (AR) and its variants’ expression along with the downstream signals are mostly important for disease progression. However, the mechanism for marked increases of AR signals and its expression is still unclear. Here, we revealed that various spliceosome genes are aberrantly induced by RNA-binding protein PSF, leading to enhancement of the splicing activities for AR expression. Our high-speed sequence analyses identified global PSF-binding transcripts. PSF was shown to stabilize and activate key long noncoding RNAs and AR-regulated gene expressions in prostate cancer cells. Interestingly, mRNAs of spliceosome-related genes are putative primary targets of PSF. Their gene expressions are up-regulated by PSF in hormone-refractory prostate cancer. Moreover, PSF coordinated these spliceosome proteins to form a complex to promote AR splicing and expression. Thus, targeting PSF and its related pathways implicates the therapeutic possibility for hormone-refractory prostate cancer.

scholarly journals RNA-binding protein DDX3 mediates posttranscriptional regulation of androgen receptor: A mechanism of castration resistance

2020 ◽  
Vol 117 (45) ◽  
pp. 28092-28101 ◽  
Author(s):  
Jordan E. Vellky ◽  
Sean T. McSweeney ◽  
Emily A. Ricke ◽  
William A. Ricke
Keyword(s):  
Prostate Cancer ◽  
Androgen Receptor ◽  
Protein Expression ◽  
Messenger Rna ◽  
Posttranscriptional Regulation ◽  
Rna Binding ◽  
Binding Protein ◽  
Rna Binding Protein ◽  
Protein Translation

Prostate cancer (CaP) driven by androgen receptor (AR) is treated with androgen deprivation; however, therapy failure results in lethal castration-resistant prostate cancer (CRPC). AR-low/negative (ARL/−) CRPC subtypes have recently been characterized and cannot be targeted by hormonal therapies, resulting in poor prognosis. RNA-binding protein (RBP)/helicase DDX3 (DEAD-box helicase 3 X-linked) is a key component of stress granules (SG) and is postulated to affect protein translation. Here, we investigated DDX3-mediated posttranscriptional regulation of AR mRNA (messenger RNA) in CRPC. Using patient samples and preclinical models, we objectively quantified DDX3 and AR expression in ARL/− CRPC. We utilized CRPC models to identify DDX3:AR mRNA complexes by RNA immunoprecipitation, assess the effects of DDX3 gain/loss-of-function on AR expression and signaling, and address clinical implications of targeting DDX3 by assessing sensitivity to AR-signaling inhibitors (ARSI) in CRPC xenografts in vivo. ARL/− CRPC expressed abundant AR mRNA despite diminished levels of AR protein. DDX3 protein was highly expressed in ARL/− CRPC, where it bound to AR mRNA. Consistent with a repressive regulatory role, DDX3 localized to cytoplasmic puncta with SG marker PABP1 in CRPC. While induction of DDX3-nucleated SGs resulted in decreased AR protein expression, inhibiting DDX3 was sufficient to restore 1) AR protein expression, 2) AR signaling, and 3) sensitivity to ARSI in vitro and in vivo. Our findings implicate the RBP protein DDX3 as a mechanism of posttranscriptional regulation for AR in CRPC. Clinically, DDX3 may be targetable for sensitizing ARL/− CRPC to AR-directed therapies.

scholarly journals The RNA-binding Protein HuR Opposes the Repression ofERBB-2Gene Expression by MicroRNA miR-331-3p in Prostate Cancer Cells

2011 ◽  
Vol 286 (48) ◽  
pp. 41442-41454 ◽  
Author(s):  
Michael R. Epis ◽  
Andrew Barker ◽  
Keith M. Giles ◽  
Dianne J. Beveridge ◽  
Peter J. Leedman
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Rna Binding ◽  
Binding Protein ◽  
Rna Binding Protein ◽  
Prostate Cancer Cells

The RNA-binding protein FXR1 modulates prostate cancer progression by regulating FBXO4

2019 ◽  
Vol 19 (3) ◽  
pp. 487-496 ◽  
Author(s):  
Hongwen Cao ◽  
Renjie Gao ◽  
Chao Yu ◽  
Lei Chen ◽  
Yigeng Feng
Keyword(s):  
Prostate Cancer ◽  
Cancer Progression ◽  
Rna Binding ◽  
Binding Protein ◽  
Rna Binding Protein ◽  
Prostate Cancer Progression
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