Impact of RNA‑binding motif 3 expression on the whole transcriptome of prostate cancer cells: An RNA sequencing study

Abstract Background Prostate cancer is one of the most common malignant cancers with the second highest global rate of mortality in men. During the early stages of disease progression, tumour growth is local and androgen-dependent. Despite treatment, a large percentage of patients develop androgen-independent prostate cancer, which often results in metastases, a leading cause of mortality in these patients. Our previous work on the RNA-binding protein Staufen1 demonstrated its novel role in cancer biology, and in particular rhabdomyosarcoma tumorigenesis. To build upon this work, we have focused on the role of Staufen1 in other forms of cancer and describe here the novel and differential roles of Staufen1 in prostate cancer. Methods Using a cell-based approach, three independent prostate cancer cell lines with different characteristics were used to evaluate the expression of Staufen1 in human prostate cancer relative to control prostate cells. The functional impact of Staufen1 on several key oncogenic features of prostate cancer cells including proliferation, apoptosis, migration and invasion were systematically investigated. Results We show that Staufen1 levels are increased in all human prostate cancer cells examined in comparison to normal prostate epithelial cells. Furthermore, Staufen1 differentially regulates growth, migration, and invasion in the various prostate cancer cells assessed. In LNCaP prostate cancer cells, Staufen1 regulates cell proliferation through mTOR activation. Conversely, Staufen1 regulates migration and invasion of the highly invasive, bone metastatic-derived, PC3 prostate cells via the activation of focal adhesion kinase. Conclusions Collectively, these results show that Staufen1 has a direct impact in prostate cancer development and further demonstrate that its functions vary amongst the prostate cancer cell types. Accordingly, Staufen1 represents a novel target for the development of much-needed therapeutic strategies for prostate cancer.

Download Full-text

RNA sequencing reveals upregulation of a transcriptomic program associated with stemness in metastatic prostate cancer cells selected for taxane resistance

Oncotarget ◽

10.18632/oncotarget.25744 ◽

2018 ◽

Vol 9 (54) ◽

pp. 30363-30384 ◽

Cited By ~ 6

Author(s):

Christina K. Cajigas-Du Ross ◽

Shannalee R. Martinez ◽

Leanne Woods-Burnham ◽

Alfonso M. Durán ◽

Sourav Roy ◽

...

Keyword(s):

Prostate Cancer ◽

Cancer Cells ◽

Rna Sequencing ◽

Metastatic Prostate Cancer ◽

Prostate Cancer Cells ◽

Taxane Resistance

Download Full-text

Knockdown of long noncoding RNA AC245100.4 inhibits the tumorigenesis of prostate cancer cells via the STAT3/NR4A3 axis

Epigenomics ◽

10.2217/epi-2021-0293 ◽

2021 ◽

Author(s):

Chi Liu ◽

Ping Lin ◽

Jiabin Zhao ◽

Hui Xie ◽

Rou Li ◽

...

Keyword(s):

Prostate Cancer ◽

Cancer Cells ◽

Rna Sequencing ◽

Long Noncoding Rna ◽

Noncoding Rna ◽

Transcriptional Repressor ◽

Sequencing Analysis ◽

Loss Of Function ◽

Prostate Cancer Cells ◽

Rna Immunoprecipitation

Aim: To explore the role and mechanism of long noncoding RNA AC245100.4 and NR4A3 in prostate cancer (PCa). Methods: RNA-sequencing analysis was used to detect the downstream genes of AC245100.4. A series of gain- and loss-of-function approaches were used to investigate the roles of AC245100.4 and NR4A3. RNA immunoprecipitation was performed to examine the interaction between AC245100.4 and STAT3. Results: AC245100.4 was significantly upregulated in PCa cells and tissues. Knockdown of AC21500.4 significantly inhibited the tumorigenesis of PCa cells. Mechanistically, AC245100.4 deregulated the transcription of NR4A3 via increasing p-STAT3, which acted as a transcriptional repressor of NR4A3. Conclusion: Knockdown of lncRNA AC245100.4 inhibits the tumorigenesis of PCa cells via the STAT3/ NR4A3 axis.

Download Full-text

Abstract 2800: Target RNA sequencing analysis of hypoxia induced expression of stem cell genes in primary cultures of prostate cancer cells

10.1158/1538-7445.am2016-2800 ◽

2016 ◽

Author(s):

Hong Yin ◽

Adam H. Greer ◽

Glenn Mills

Keyword(s):

Prostate Cancer ◽

Stem Cell ◽

Cancer Cells ◽

Rna Sequencing ◽

Primary Cultures ◽

Sequencing Analysis ◽

Prostate Cancer Cells ◽

Induced Expression ◽

Target Rna

Download Full-text

Regulation of circGOLPH3 and its binding protein CBX7 on the proliferation and apoptosis of prostate cancer cells

Bioscience Reports ◽

10.1042/bsr20200936 ◽

2020 ◽

Vol 40 (12) ◽

Author(s):

Lifeng Gong ◽

Yu Tang ◽

Li Jiang ◽

Wei Tang ◽

Shengjun Luo

Keyword(s):

Prostate Cancer ◽

Cancer Cells ◽

Rna Binding ◽

Prostate Cancer Cell ◽

Binding Protein ◽

Cancer Cell Proliferation ◽

Proliferative Capacity ◽

Prostate Cancer Cells ◽

Proliferation And Apoptosis ◽

Cellular Apoptosis

Abstract To clarify the mechanism of circGOLPH3 regulation on prostate cancer cells, we performed an overexpression and interference circGOLPH3 assay in prostate cancer cells PC-3 and then evaluated cellular viability, proliferation, cell cycle, and apoptosis of prostate cancer cells by MTT, CCK8, Edu stain, TUNEL stain, and flow cytometry. Binding proteins of CircGOLPH3 were identified by RNA pull-down, mass spectrometry, and RNA-binding protein immunoprecipitation (RIP) assays. The expressions of CircGOLPH3 and CBX7 were measured by qRT-PCR. The results showed that after overexpression of circGOLPH3, the proliferative capacity and the viability of PC-3cells were significantly improved, whereas apoptosis was inhibited. CircGOLPH3 could bind to the CBX7 protein that was highly expressed in the PC-3 cell. Additionally, a functional test on CBX7 showed that the CBX7 overexpression notably improved the proliferative capacity and the viability of PC-3 cells and decreased cellular apoptosis, which was consistent with the effects of circGOLPH3. The validated the present study that circGOLPH3 and its binding protein CBX7 can promote prostate cancer cell proliferation and inhibit apoptosis.

Download Full-text

RNA sequencing data of human prostate cancer cells treated with androgens

Data in Brief ◽

10.1016/j.dib.2019.104372 ◽

2019 ◽

Vol 25 ◽

pp. 104372 ◽

Cited By ~ 5

Author(s):

Raghavendra Tejo Karthik Poluri ◽

Charles Joly Beauparlant ◽

Arnaud Droit ◽

Étienne Audet-Walsh

Keyword(s):

Prostate Cancer ◽

Cancer Cells ◽

Rna Sequencing ◽

Human Prostate ◽

Human Prostate Cancer ◽

Prostate Cancer Cells ◽

Sequencing Data

Download Full-text

Cerebral cavernous malformation 1 determines YAP/TAZ signaling dependent metastatic hallmarks of prostate cancer cells

10.1101/2020.04.23.057778 ◽

2020 ◽

Author(s):

Sangryoung Park ◽

Ho-Yong Lee ◽

Hansol Park ◽

Young Seok Ju ◽

Jayoung Kim ◽

...

Keyword(s):

Prostate Cancer ◽

Cancer Cells ◽

Cancer Progression ◽

Cancer Metastasis ◽

Cavernous Malformation ◽

Predictive Biomarker ◽

Cerebral Cavernous Malformation ◽

Binding Motif ◽

Prostate Cancer Cells ◽

Prostate Cancer Metastasis

AbstractEnhanced Yes-associated protein (YAP)/transcriptional co-activator with PDZ-binding motif (TAZ) signaling is correlated with the extraprostatic extension of prostate cancer. However, the mechanism by which YAP/TAZ signaling becomes hyperactive and drives prostate cancer progression is currently unclear. In this study, we demonstrated that CCM1 induces the metastasis of multiple types of prostate cancer cells by regulating YAP/TAZ signaling. Mechanistically, CCM1, a gene mutated in cerebral cavernous malformation, suppresses DDX5, which regulates the PLK1-mediated suppression of YAP/TAZ signaling, indicating that CCM1 and DDX5 are novel upstream regulators of YAP/TAZ signaling. We also revealed that higher expression of CCM1, which is uniquely found in advanced prostate cancer, is inversely correlated with metastasis-free and overall survival in patients with prostate cancer. Our findings highlight the importance of CCM1-DDX5-PLK1-YAP/TAZ signaling in the metastasis of prostate cancer cells.Statement of SignificanceOur analysis of CCM1 expression and function represents a candidate predictive biomarker for prostate cancer metastasis and provides an evidence that abnormality of CCM1 can be pathogenic in prostate cancer. Importantly, CCM1 regulation of metastasis progression appears to a common molecular event in metastatic prostate cancer cells arising in disparate genetic backgrounds.

Download Full-text