scholarly journals Comparative Proteomics Uncovers Correlated Signaling Network and Potential Biomarkers for Progression of Prostate Cancer

2017 ◽  
Vol 41 (1) ◽  
pp. 1-9 ◽  
Author(s):  
Jianzhong Ai ◽  
Yi Lu ◽  
Qiang Wei ◽  
Hong Li
Keyword(s):  
Prostate Cancer ◽  
Cell Migration ◽  
Cancer Progression ◽  
Quantitative Proteomics ◽  
Tumor Metastasis ◽  
Metastatic Prostate Cancer ◽  
Bioinformatics Analysis ◽  
Mrna Level ◽  
Tumor Cell Migration ◽  
Differential Proteins

Background/Aims: Prostate cancer is one of the most common cancers for males worldwide, and it is prone to show the metastatic foci in lymph node and bone with high mortality. To date, the potential mechanism and the corresponding biomarkers for metastatic prostate cancer are still lacking. Hence, our study aims to clarify the mechanism of prostate cancer progression and identify the useful biomarkers for metastatic prostate cancer. Methods: The proteins and network tightly associated with tumor metastasis were identified using quantitative proteomics. Furthermore, the mRNA level of differential expressed proteins were confirmed using qRT-PCR, and the functional cluster analysis was performed using String and Cytoscape. Results: Totally, our study identified 203 differential proteins closely associated with tumor cell migration, and the mRNA expression of those proteins were verified by qPCR. Moreover, the migration associated molecular network was established using bioinformatics analysis. Conclusion: These data raveled the critical proteins for the cell migration of prostate cancer, and identified the potential markers for diagnosing the metastasis of prostate cancer.

scholarly journals TUG1 promotes prostate cancer progression by acting as a ceRNA of miR-26a

2018 ◽  
Vol 38 (5) ◽  
Author(s):  
Bin Yang ◽  
Xiaodi Tang ◽  
Zhixin Wang ◽  
Daju Sun ◽  
Xin Wei ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Progression ◽  
Migration And Invasion ◽  
Tumor Cell Migration ◽  
Real Time Quantitative Pcr ◽  
Non Coding Rna ◽  
Key Aspects ◽  
And Function ◽  
First Time ◽  
Long Non Coding Rna

Previous studies have demonstrated that taurine-upregulated gene 1 (TUG1) was aberrantly expressed and involved in multiple types of cancer; however, the expression profile and potential role of TUG1 in prostate cancer (PCa) remains unclear. The aim of the present study was to evaluate the expression and function of TUG1 in PCa. In the present study, we analyzed TUG1 expression levels of PCa patients in tumor and adjacent normal tissue by real-time quantitative PCR. Knockdown of TUG1 by RNAi was performed to explore its roles in cell proliferation, migration, and invasion. Here we report, for the first time, that TUG1 promotes tumor cell migration, invasion, and proliferation in PCa by working in key aspects of biological behaviors. TUG1 could negatively regulate the expression of miR-26a in PCa cells. The bioinformatics prediction revealed putative miR-26a-binding sites within TUG1 transcripts. In conclusion, our study suggests that long non-coding RNA (lncRNA) TUG1 acts as a functional oncogene in PCa development.

scholarly journals Neutrophils are mediators of metastatic prostate cancer progression in bone

2020 ◽  
Vol 69 (6) ◽  
pp. 1113-1130 ◽  
Author(s):  
Diane L. Costanzo-Garvey ◽  
Tyler Keeley ◽  
Adam J. Case ◽  
Gabrielle F. Watson ◽  
Massar Alsamraae ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Progression ◽  
Metastatic Prostate Cancer ◽  
Prostate Cancer Progression

scholarly journals Clinical and genomic analysis of metastatic prostate cancer progression with a background of postoperative biochemical recurrence

2015 ◽  
Vol 116 (4) ◽  
pp. 556-567 ◽  
Author(s):  
Mohammed Alshalalfa ◽  
Anamaria Crisan ◽  
Ismael A. Vergara ◽  
Mercedeh Ghadessi ◽  
Christine Buerki ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Progression ◽  
Biochemical Recurrence ◽  
Metastatic Prostate Cancer ◽  
Genomic Analysis ◽  
Prostate Cancer Progression

scholarly journals A Splicing Variant of the Androgen Receptor Detected in a Metastatic Prostate Cancer Exhibits Exclusively Cytoplasmic Actions

Endocrinology ◽  
2007 ◽  
Vol 148 (9) ◽  
pp. 4334-4343 ◽  
Author(s):  
Monika Jagla ◽  
Marie Fève ◽  
Pascal Kessler ◽  
Gaëlle Lapouge ◽  
Eva Erdmann ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Androgen Receptor ◽  
Dna Binding ◽  
Cancer Progression ◽  
Metastatic Prostate Cancer ◽  
Transcriptional Activity ◽  
Target Genes ◽  
Nuclear Translocation ◽  
Splicing Variant ◽  
Activation Of Transcription

The androgen receptor (AR) is a ligand-activated transcription factor that displays genomic actions characterized by binding to androgen-response elements in the promoter of target genes as well as nongenomic actions that do not require nuclear translocation and DNA binding. In this study, we report exclusive cytoplasmic actions of a splicing variant of the AR detected in a metastatic prostate cancer. This AR variant, named AR23, results from an aberrant splicing of intron 2, wherein the last 69 nucleotides of the intronic sequence are retained, leading to the insertion of 23 amino acids between the two zinc fingers in the DNA-binding domain. We show that the nuclear entry of AR23 upon dihydrotestosterone (DHT) stimulation is impaired. Alternatively, DHT-activated AR23 forms cytoplasmic and perinuclear aggregates that partially colocalize with the endoplasmic reticulum and are devoid of genomic actions. However, in LNCaP cells, this cytoplasmic DHT-activated AR23 remains partially active as evidenced by the activation of transcription from androgen-responsive promoters, the stimulation of NF-κB transcriptional activity and by the decrease of AP-1 transcriptional activity. Our data reveal novel cytoplasmic actions for this splicing AR variant, suggesting a contribution in prostate cancer progression.

scholarly journals Serum Methionine Metabolites Are Risk Factors for Metastatic Prostate Cancer Progression

PLoS ONE ◽  
2011 ◽  
Vol 6 (8) ◽  
pp. e22486 ◽  
Author(s):  
Sally Stabler ◽  
Tatsuki Koyama ◽  
Zhiguo Zhao ◽  
Magaly Martinez-Ferrer ◽  
Robert H. Allen ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Risk Factors ◽  
Cancer Progression ◽  
Metastatic Prostate Cancer ◽  
Prostate Cancer Progression

scholarly journals PUM1 represses CDKN1B translation and contributes to prostate cancer progression

2021 ◽  
Author(s):  
Eugene Yujun Xu
Keyword(s):  
Prostate Cancer ◽  
Cell Proliferation ◽  
Protein Expression ◽  
Cancer Cell ◽  
Cancer Progression ◽  
Translational Control ◽  
Rna Binding ◽  
Prostate Cancer Cell ◽  
Mrna Level ◽  
Critical Role

Posttranscriptional regulation of cancer gene expression programs plays a vital role in carcinogenesis; identifying the critical regulators of tumorigenesis and their molecular targets may provide novel strategies for cancer diagnosis and therapeutics. Highly conserved RNA binding protein PUM1 regulates mouse growth and cell proliferation, propelling us to examine its role in cancer. We found human PUM1 is highly expressed in a diverse group of cancer, including prostate cancer; enhanced PUM1 expression is also correlated with reduced survival among prostate cancer patients. Detailed expression analysis in twenty prostate cancer tissues showed enhanced expression of PUM1 at mRNA and protein levels. Knockdown of PUM1 reduced prostate cancer cell proliferation and colony formation, and subcutaneous injection of PUM1 knockdown cells led to reduced tumor size. Downregulation of PUM1 in prostate cancer cells consistently elevated CDKN1B protein expression through increased translation but did not impact its mRNA level, while overexpression of PUM1 reduced CDKN1B protein level. Our finding established a critical role of PUM1 mediated translational control, particularly the PUM1-CDKN1B axis, in prostate cancer cell growth and tumorigenesis. We proposed that PUM1-CDKN1B regulatory axis may represent a novel mechanism for the loss of CDKN1B protein expression in diverse cancers and could be potential targets for therapeutics development.

scholarly journals LncRNA PAINT is Associated with Aggressive Prostate Cancer and Dysregulation of Slug and Related Genes

2020 ◽  
Author(s):  
Md Faqrul Hasan ◽  
Kavya Ganapathy ◽  
Jiao Sun ◽  
Khatib Ayman ◽  
Thomas Andl ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Migration ◽  
Cancer Progression ◽  
Kinase Inhibitor ◽  
Epithelial Mesenchymal Transition ◽  
Ectopic Expression ◽  
S Phase ◽  
Aberrant Expression ◽  
Mesenchymal Transition ◽  
Phase Progression

AbstractLong non-coding RNAs (lncRNAs) play regulatory roles in cellular processes and their aberrant expression may drive cancer progression. Here we report the function of a lncRNA PAINT (Prostate Cancer Associated Intergenic Non-Coding Transcript) in promoting prostate cancer (PCa) progression. Upregulation of PAINT was noted in advanced stage and metastatic PCa. Inhibition of PAINT decreased cell proliferation, S-phase progression, increased expression of apoptotic markers, and improved sensitivity to docetaxel and Aurora kinase inhibitor VX-680. Inhibition of PAINT decreased cell migration and reduced expression of Slug and Vimentin. Ectopic expression of PAINT suppressed E-cadherin, increased S-phase progression and cell migration. PAINT expression in PCa cells induced larger colony formation and higher expression of mesenchymal markers. Transcriptome analysis followed by qRT-PCR validation showed differentially expressed genes involved in epithelial mesenchymal transition (EMT), apoptosis and drug resistance in PAINT-expressing cells. Our study establishes an oncogenic function of PAINT in PCa.

scholarly journals The PHLPP2 phosphatase is a druggable driver of prostate cancer progression

2019 ◽  
Vol 218 (6) ◽  
pp. 1943-1957 ◽  
Author(s):  
Dawid G. Nowak ◽  
Ksenya Cohen Katsenelson ◽  
Kaitlin E. Watrud ◽  
Muhan Chen ◽  
Grinu Mathew ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Progression ◽  
Metastatic Prostate Cancer ◽  
Genetically Engineered ◽  
Phosphatase Inhibitors ◽  
Genetically Engineered Mouse Model ◽  
Key Driver ◽  
The Common ◽  
Chromosome 16Q ◽  
Mutant Cells

Metastatic prostate cancer commonly presents with targeted, bi-allelic mutations of the PTEN and TP53 tumor suppressor genes. In contrast, however, most candidate tumor suppressors are part of large recurrent hemizygous deletions, such as the common chromosome 16q deletion, which involves the AKT-suppressing phosphatase PHLPP2. Using RapidCaP, a genetically engineered mouse model of Pten/Trp53 mutant metastatic prostate cancer, we found that complete loss of Phlpp2 paradoxically blocks prostate tumor growth and disease progression. Surprisingly, we find that Phlpp2 is essential for supporting Myc, a key driver of lethal prostate cancer. Phlpp2 dephosphorylates threonine-58 of Myc, which renders it a limiting positive regulator of Myc stability. Furthermore, we show that small-molecule inhibitors of PHLPP2 can suppress MYC and kill PTEN mutant cells. Our findings reveal that the frequent hemizygous deletions on chromosome 16q present a druggable vulnerability for targeting MYC protein through PHLPP2 phosphatase inhibitors.

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