AS1 expression in prostate cancer and its effects on proliferation and invasion of prostate cancer cells

This paper aimed at investigating AS1 expression in prostate cancer (PCa) and its effects on the proliferation and invasion of prostate cancer cells (PCCs). The prostate tissues and the matched adjacent normal prostate tissues excised and preserved during radical prostatectomy in our hospital were collected. The LncRNA NCK1-AS1 expression was detected. PCa patients were followed up for three years to analyze their prognosis. The correlation of LncRNA NCK1-AS1 expression with clinicopathological features was analyzed. Human normal prostate cells and human PCCs were selected, in which LncRNA NCK1-AS1 expression was tested to screen and then transfect the cells. Cell proliferation, invasion and migration were detected. Cell cycles and apoptosis were analyzed. Compared with the adjacent normal tissues, LncRNA NCK1-AS1 was highly expressed in the prostate cancer tissues. Its expression was remarkably different in those with different stages of TNM and with lymphatic metastasis or not. The prognosis of patients with high LncRNA NCK1-AS1 expression was remarkably poorer than that of those with low expression. Compared with the human normal prostate cells, LncRNA NCK1-AS1 expression in the human PCCs remarkably rose, with the greatest difference in 22Rv1 cells. Compared with the Blank group, cell proliferation and the number of plate cloned cells remarkably reduced in the sh-NCK1-AS1 group. Additionally, in this group, the number of invasive and migratory cells remarkably reduced; the expression of invasion-related protein E-cadherin remarkably rose but that of MMP-2 remarkably reduced; cell cycles were arrested and the expression of cycle-related proteins (CDK4, CDK6, cyclin D1) remarkably reduced; the apoptotic rate and the expression of apoptosis-related protein Bax remarkably rose. LncRNA NCK1-AS1 is highly expressed in PCa, so its down-regulation can inhibit PCCs from proliferating and reduce the number of invasive cells.

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SOX30, a target gene of miR-653-5p, represses the proliferation and invasion of prostate cancer cells through inhibition of Wnt/β-catenin signaling

Cellular & Molecular Biology Letters ◽

10.1186/s11658-019-0195-4 ◽

2019 ◽

Vol 24 (1) ◽

Cited By ~ 4

Author(s):

Qiang Fu ◽

Zhenye Sun ◽

Fan Yang ◽

Tianci Mao ◽

Yanyao Gao ◽

...

Keyword(s):

Prostate Cancer ◽

Cancer Cells ◽

Cancer Cell ◽

Target Gene ◽

Prostate Cancer Cell ◽

Luciferase Reporter ◽

Prostate Cancer Cells ◽

Normal Prostate ◽

Proliferation And Invasion ◽

In Cells

Abstract Background Sex-determining region Y-box containing gene 30 (SOX30) is a newly identified tumor-associated gene in several types of cancer. However, whether SOX30 is involved in the development and progression of prostate cancer remains unknown. This study investigated the potential role of SOX30 in prostate cancer. Methods Prostate cancer cell lines and a normal prostate epithelial cell line were used for the experiments. The expression of SOX30 was determined using quantitative real-time PCR and western blot analysis. The malignant cellular behaviors of prostate cancer were assessed using the Cell Counting Kit-8, colony formation and Matrigel invasion assays. The miRNA–mRNA interaction was validated using the dual-luciferase reporter assay. Results SOX30 expression was lower in cells of prostate cancer lines than in cells of the normal prostate epithelial line. Its overexpression repressed the proliferation and invasion of prostate cancer cells. SOX30 was identified as a target gene of microRNA-653-5p (miR-653-5p), which is upregulated in prostate cancer tissues. MiR-653-5p overexpression decreased SOX30 expression, while its inhibition increased SOX30 expression in prostate cancer cells. MiR-653-5p inhibition also markedly restricted prostate cancer cell proliferation and invasion. SOX30 overexpression or miR-653-5p inhibition significantly reduced β-catenin expression and downregulated the activation of Wnt/β-catenin signaling. SOX30 knockdown significantly reversed the miR-653-5p inhibition-mediated inhibitory effect on the proliferation, invasion and Wnt/β-catenin signaling in prostate cancer cells. Conclusions These results reveal a tumor suppressive function for SOX30 in prostate cancer and confirmed the gene as a target of miR-653-5p. SOX30 upregulation due to miR-653-5p inhibition restricted the proliferation and invasion of prostate cancer cells, and this was associated with Wnt/β-catenin signaling suppression. These findings highlight the importance of the miR-653-5p–SOX30–Wnt/β-catenin signaling axis in prostate cancer progression.

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The inhibition of p85αPI3KSer83 phosphorylation prevents cell proliferation and invasion in prostate cancer cells

Journal of Cellular Biochemistry ◽

10.1002/jcb.24558 ◽

2013 ◽

Vol 114 (9) ◽

pp. 2114-2119 ◽

Cited By ~ 7

Author(s):

Antonia Feola ◽

Annamaria Cimini ◽

Francesca Migliucci ◽

Rosamaria Iorio ◽

Candida Zuchegna ◽

...

Keyword(s):

Prostate Cancer ◽

Cell Proliferation ◽

Cancer Cells ◽

Prostate Cancer Cells ◽

Proliferation And Invasion

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Abstract 5340: MicroRNA-720 promotes cell proliferation and invasion in prostate cancer cells.

10.1158/1538-7445.am2013-5340 ◽

2013 ◽

Author(s):

Soichiro Yamamura ◽

Takeshi Chiyomaru ◽

Shinichiro Fukuhara ◽

Sharanjot Saini ◽

Shahana Majid ◽

...

Keyword(s):

Prostate Cancer ◽

Cell Proliferation ◽

Cancer Cells ◽

Prostate Cancer Cells ◽

Proliferation And Invasion

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KLF5 Is Crucial for Androgen-AR Signaling to Transactivate Genes and Promote Cell Proliferation in Prostate Cancer Cells

Cancers ◽

10.3390/cancers12030748 ◽

2020 ◽

Vol 12 (3) ◽

pp. 748 ◽

Cited By ~ 1

Author(s):

Juan Li ◽

Baotong Zhang ◽

Mingcheng Liu ◽

Xing Fu ◽

Xinpei Ci ◽

...

Keyword(s):

Prostate Cancer ◽

Cell Proliferation ◽

Cancer Cells ◽

Transcriptional Activity ◽

Prostate Cancer Cells ◽

Normal Prostate ◽

Promote Cell Proliferation ◽

Therapeutic Opportunity

Androgen/androgen receptor (AR) signaling drives both the normal prostate development and prostatic carcinogenesis, and patients with advanced prostate cancer often develop resistance to androgen deprivation therapy. The transcription factor Krüppel-like factor 5 (KLF5) also regulates both normal and cancerous development of the prostate. In this study, we tested whether and how KLF5 plays a role in the function of AR signaling in prostate cancer cells. We found that KLF5 is upregulated by androgen depending on AR in LNCaP and C4-2B cells. Silencing KLF5, in turn, reduced AR transcriptional activity and inhibited androgen-induced cell proliferation and tumor growth in vitro and in vivo. Mechanistically, KLF5 occupied the promoter of AR, and silencing KLF5 repressed AR transcription. In addition, KLF5 and AR physically interacted with each other to regulate the expression of multiple genes (e.g., MYC, CCND1 and PSA) to promote cell proliferation. These findings indicate that, while transcriptionally upregulated by AR signaling, KLF5 also regulates the expression and transcriptional activity of AR in androgen-sensitive prostate cancer cells. The KLF5-AR interaction could provide a therapeutic opportunity for the treatment of prostate cancer.

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Increased distributional variance of mitochondrial DNA content associated with prostate cancer cells as compared with normal prostate cells

The Prostate ◽

10.1002/pros.20697 ◽

2008 ◽

Vol 68 (4) ◽

pp. 408-417 ◽

Cited By ~ 55

Author(s):

Takatsugu Mizumachi ◽

Levan Muskhelishvili ◽

Akihiro Naito ◽

Jun Furusawa ◽

Chun-Yang Fan ◽

...

Keyword(s):

Prostate Cancer ◽

Mitochondrial Dna ◽

Cancer Cells ◽

Dna Content ◽

Prostate Cancer Cells ◽

Normal Prostate ◽

Prostate Cells ◽

Mitochondrial Dna Content

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DNA licensing as a novel androgen receptor mediated therapeutic target for prostate cancer

Endocrine Related Cancer ◽

10.1677/erc-08-0205 ◽

2009 ◽

Vol 16 (2) ◽

pp. 325-332 ◽

Cited By ~ 28

Author(s):

Jason M D'Antonio ◽

Donald J Vander Griend ◽

John T Isaacs

Keyword(s):

Prostate Cancer ◽

Cell Cycle ◽

Cell Proliferation ◽

Androgen Receptor ◽

Dna Replication ◽

Cancer Cells ◽

Cancer Biology ◽

Prostate Cancer Cells ◽

Normal Prostate ◽

Malignant Prostate

During middle G1 of the cell cycle origins of replication orchestrate the ordered assembly of the pre-replication complex (pre-RC), allowing licensing of DNA required for DNA replication. Cyclin-dependent kinase activation of the pre-RC facilitates the recruitment of additional signaling factors, which triggers DNA unwinding and replication, while limiting such DNA replication to once and only once per cell cycle. For both the normal and malignant prostate, androgen is the major stimulator of cell proliferation and thus DNA replication. In both cases, the binding of androgen to the androgen receptor (AR) is required. However, the biochemical cascade involved in such AR-stimulated cell proliferation and DNA synthesis is dramatically different in normal versus malignant prostate cells. In normal prostate, AR-stimulated stromal cell paracrine secretion of andromedins stimulates DNA replication within prostatic epithelial cells, in which AR functions as a tumor suppressor gene by inducing proliferative quiescence and terminal differentiation. By direct contrast, nuclear AR in prostate cancer cells autonomously stimulates continuous growth via incorporation of AR into the pre-RC. Such a gain of function by AR-expressing prostate cancer cells requires that AR be efficiently degraded during mitosis since lack of such degradation leads to re-licensing problems, resulting in S-phase arrest during the subsequent cell cycle. Thus, acquisition of AR as part of the licensing complex for DNA replication represents a paradigm shift in how we view the role of AR in prostate cancer biology, and introduces a novel vulnerability in AR-expressing prostate cancer cells apt for therapeutic intervention.

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Annexin-A7 protects normal prostate cells and induces distinct patterns of RB-associated cytotoxicity in androgen-sensitive and -resistant prostate cancer cells

International Journal of Cancer ◽

10.1002/ijc.24592 ◽

2009 ◽

Vol 125 (11) ◽

pp. 2528-2539 ◽

Cited By ~ 17

Author(s):

Yelizaveta Torosyan ◽

Olga Simakova ◽

Shanmugam Naga ◽

Katerina Mezhevaya ◽

Ximena Leighton ◽

...

Keyword(s):

Prostate Cancer ◽

Cancer Cells ◽

Prostate Cancer Cells ◽

Normal Prostate ◽

Prostate Cells ◽

Annexin A7

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MicroRNA-590-3p promotes cell proliferation and invasion by targeting inositol polyphosphate 4-phosphatase type II in human prostate cancer cells

Tumor Biology ◽

10.1177/1010428317695941 ◽

2017 ◽

Vol 39 (3) ◽

pp. 101042831769594 ◽

Cited By ~ 7

Author(s):

Haiwen Chen ◽

Qidong Luo ◽

Hongliang Li

Keyword(s):

Prostate Cancer ◽

Cell Proliferation ◽

Tumor Growth ◽

Cancer Cells ◽

Prostate Cancer Cell ◽

Type Ii ◽

Human Prostate Cancer ◽

Inositol Polyphosphate ◽

Prostate Cancer Cells ◽

Proliferation And Invasion

Inositol polyphosphate 4-phosphatase type II emerges as a tumor suppressor in prostate cancer, and its loss of expression is associated with poor prognosis for prostate cancer. However, the mechanism of downregulation of inositol polyphosphate 4-phosphatase type II in prostate cancer development has not yet been fully clarified. In this study, microRNA-590-3p was found to be upregulated in both prostate cancer tissues and cell lines. Overexpression of microRNA-590-3p by microRNA-590-3p mimics promoted prostate cancer cell proliferation and invasion and accelerated the growth of xenografted tumors, while microRNA-590-3p inhibitors contributed to inhibition of cellular proliferation and invasion as well as tumor growth. A dual-luciferase reporter assay and expression analysis further confirmed that inositol polyphosphate 4-phosphatase type II was a direct target of microRNA-590-3p. Enforced expression of microRNA-590-3p led to repression of inositol polyphosphate 4-phosphatase type II messenger RNA and protein expression, as well as upregulation of p-Akt, p-FoxO3a, and cyclin D1 and downregulation of p21 expression in prostate cancer cell lines. Overexpression of inositol polyphosphate 4-phosphatase type II could reduce microRNA-590-3p-induced cell proliferation and invasion as well as tumor growth, and decrease microRNA-590-3p-mediated upregulation of cyclin D1 and downregulation of p21 expression in prostate cancer cells. Taken together, our findings reveal that microRNA-590-3p is a potential onco-microRNA that participates in carcinogenesis of human prostate cancer by suppressing inositol polyphosphate 4-phosphatase type II expression and involving the Akt/FoxO3a pathway. MicroRNA-590-3p may represent a potential therapeutic target for prostate cancer patients.

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