scholarly journals Circular RNA circ_0057558 Controls Prostate Cancer Cell Proliferation Through Regulating miR-206/USP33/c-Myc Axis

2021 ◽  
Vol 9 ◽  
Author(s):  
Tao Ding ◽  
Yanjun Zhu ◽  
Huimin Jin ◽  
Ping Zhang ◽  
Jianming Guo ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Negative Correlation ◽  
Bioinformatics Analysis ◽  
Prostate Cancer Cell ◽  
Prostate Cancer Cells ◽  
Cancer Tissues

We previously reported the elevated expression of circ_0057558 in prostate cancer tissues and cell lines. Here, we aimed to determine the biological function of circ_0057558 in prostate cancer. In the current study, circ_0057558 knockdown in prostate cancer cells significantly repressed cell proliferation and colony formation, but promoted cell arrest and enhanced the sensitivity to docetaxel. Bioinformatics analysis prediction and RNA-pull down assay identified miR-206 as the potential binding miRNA of circ_0057558. A negative correlation was observed between the expression of miR-206 and circ_0057558 in prostate cancer tissues. miR-206 mimics rescued the function of circ_0057558 overexpression on prostate cancer cells. Further, the bioinformatics analysis and luciferase assay suggested that miR-206 may target ubiquitin-specific peptidase 33 (USP33). USP33 mRNA expression has negative correlation with miR-206 expression and positive correlation with circ_0057558 expression in prostate cancer tissues. USP33 overexpression partially blocked the effects of miR-206 mimics on prostate cell proliferation. USP33 could bind and deubiquitinate c-Myc. Increased c-Myc protein by circ_0057558 overexpression was partially reversed by miR-206 mimics. The proliferation inhibition activity of MYC inhibitor 361 (MYCi361) was more prominent in primary prostate cancer cells and patient-derived xenograft (PDX) model with higher level of circ_0057558. Collectively, circ_0057558 gives an impetus to cell proliferation and cell cycle control in prostate cancer cell lines by sponging miR-206 and positively regulating the transcription of the miR-206 target gene USP33.

scholarly journals miRNA-214-5p inhibits prostate cancer cell proliferation by targeting SOX4

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Guangchi Xu ◽  
Yin Meng ◽  
Lihe Wang ◽  
Bo Dong ◽  
Feifei Peng ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Target Genes ◽  
Prostate Cancer Cell ◽  
Luciferase Reporter ◽  
Prostate Cancer Cells ◽  
Cancer Tissues

Abstract Background Prostate cancer is the most common malignant tumor in men. Due to the lack of theoretical research on its pathogenic mechanism, the current cure rate is still low. miRNAs play an important role in the pathogenesis of various cancers. miRNA-214-5p plays an important role in the development of a variety of cancers. This study aims to explore the expression level of miR-214-5p in prostate cancer and make a preliminary study of its molecular mechanism in the development of prostate cancer to provide effective new strategies for the treatment of prostate cancer. Methods The target genes of miRNA-214-5p were predicted with bioinformatics technology, and the target relationship between miRNA-214-5p and its target genes was verified with dual luciferase reporter assay. RT-qPCR and Western blot were used to detect the expression levels of miRNA-214-5p and target genes in 50 clinical samples and two common prostate continuous cell lines, respectively. The targeting relationship between miRNA-214-5p and its target genes was verified with clinical data. miRNA-214-5p and miRNA-214-5p inhibitor was over-expressed in DU-145 cell lines to verify the effect of miRNA-214-5p on prostate cancer cell proliferation and SOX4 gene expression. And the mechanism of miRNA-214-5p inhibiting the proliferation of prostate cancer cells were analyzed by detecting the expression difference of downstream factors of SOX4 pathway. Bioinformatics analysis showed that miRNA-214-5p combined with SOX4 3′UTR region, and dual luciferase reporter assay further verified the reliability of the predicted results. The low expression of miRNA-214-5p was observed in prostate cancer tissues and cells, while high expression of SOX4 was observed in prostate cancer tissues and cells. Results Overexpression of miRNA-214-5p to prostate cancer cells significantly inhibited the proliferation of cancer cells, and the expression of SOX4 was inhibited in the transfected cell line. After transfection of miRNA-214-5p inhibitor into prostate cancer cells, the cell proliferation rate further increased. Meanwhile, overexpression of miRNA-214-5p effectively inhibited the expression of SOX4 downstream factors, including c-Myc, eIF4E, and CDK4. However, the specific knockdown of SOX4 through SOX4 shRNA significantly reduced the proliferation of prostate cancer cell lines. Conclusions miRNA-214-5 can inhibit the proliferation of prostate cancer cells by specifically targeting S0X4 and inhibiting the expression of growth factors downstream of this pathway.

scholarly journals How can food extracts consumed in the Mediterranean and East Asia suppress prostate cancer proliferation?

2011 ◽  
Vol 108 (3) ◽  
pp. 424-430 ◽  
Author(s):  
Mu Yao ◽  
Chanlu Xie ◽  
Maryrose Constantine ◽  
Sheng Hua ◽  
Brett D. Hambly ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Proliferation ◽  
East Asia ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Cancer Progression ◽  
Prostate Cancer Cell ◽  
Cancer Cell Proliferation ◽  
Prostate Cancer Cells ◽  
The Mediterranean

We have developed a blend of food extracts commonly consumed in the Mediterranean and East Asia, named blueberry punch (BBP), with the ultimate aim to formulate a chemoprevention strategy to inhibit prostate cancer progression in men on active surveillance protocol. We demonstrated previously that BBP inhibited prostate cancer cell proliferation in vitro and in vivo. The purpose of this study was to determine the molecular mechanism responsible for the suppression of prostate cancer cell proliferation by BBP. Treatment of lymph node-metastasised prostate cancer cells (LNCaP) and bone-metastasised prostate cancer cells (PC-3 and MDA-PCa-2b) with BBP (up to 0·8 %) for 72 h increased the percentage of cells at the G0/G1 phase and decreased those at the S and G2/M phases. The finding was supported by the reduction in the percentage of Ki-67-positive cells and of DNA synthesis measured by the incorporation of 5-ethynyl-2′-deoxyuridine. Concomitantly, BBP treatment decreased the protein levels of phosphorylated retinoblastoma, cyclin D1 and E, cyclin-dependent kinase (CDK) 4 and 2, and pre-replication complex (CDC6 and MCM7) in LNCaP and PC-3 cells, whereas CDK inhibitor p27 was elevated in these cell lines. In conclusion, BBP exerts its anti-proliferative effect on prostate cancer cells by modulating the expression and phosphorylation of multiple regulatory proteins essential for cell proliferation.

scholarly journals Human bone marrow mesenchymal stem cells-derived microRNA-205-containing exosomes impede the progression of prostate cancer through suppression of RHPN2

2019 ◽  
Vol 38 (1) ◽  
Author(s):  
Shuangjian Jiang ◽  
Chengqiang Mo ◽  
Shengjie Guo ◽  
Jintao Zhuang ◽  
Bin Huang ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Prostate Cancer Cell ◽  
Cancer Cell Proliferation ◽  
Prostate Cancer Cells ◽  
Invasion And Migration ◽  
And Migration

Abstract Background Human bone marrow mesenchymal stem cells (hBMSCs) are implicated in cancer initiation and metastasis, sometimes by releasing exosomes that mediate cell communication by delivering microRNAs (miRNAs). This study aimed to investigate the physiological mechanisms by which exosomal miR-205 derived from hBMSCs may modulate the growth of prostate cancer cells. Methods Microarray-based gene expression profiling of prostate cancer was adopted to identify differentially expressed genes and regulatory miRNAs, which identified the candidates RHPN2 and miR-205 as the study focus. Then the binding affinity between miR-205 and RHPN2 was identified using in silico analysis and luciferase activity detection. Prostate cancer cells were co-cultured with exosomes derived from hBMSCs treated with either miR-205 mimic or miR-205 inhibitor. Subsequently, prostate cancer cell proliferation, invasion, migration, and apoptosis were detected in vitro. The effects of hBMSCs-miR-205 on tumor growth were investigated in vivo. Results miR-205 was downregulated, while RHPN2 was upregulated in prostate cancer cells. RHPN2 was a target of miR-205, and upregulated miR-205 inhibited prostate cancer cell proliferation, invasion, and migration and promoted apoptosis by targeting RHPN2. Next, experiments demonstrated that hBMSCs-derived exosomes carrying miR-205 contributed to repressed prostate cancer cell proliferation, invasion, and migration and enhanced apoptosis. Furthermore, in vivo assays confirmed the inhibitory effects of hBMSCs-derived exosomal miR-205 on prostate cancer. Conclusion The hBMSCs-derived exosomal miR-205 retards prostate cancer progression by inhibiting RHPN2, suggesting that miR-205 may present a predictor and potential therapeutic target for prostate cancer.

scholarly journals Ethanolic Extract of Propolis Augments TRAIL-Induced Apoptotic Death in Prostate Cancer Cells

2011 ◽  
Vol 2011 ◽  
pp. 1-11 ◽  
Author(s):  
Ewelina Szliszka ◽  
Zenon P. Czuba ◽  
Joanna Bronikowska ◽  
Anna Mertas ◽  
Andrzej Paradysz ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Phenolic Compounds ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Prostate Cancer Cell ◽  
Ethanolic Extract ◽  
Prostate Cancer Cells ◽  
Prostate Cancer Cell Lines ◽  
Ethanolic Extract Of Propolis

Prostate cancer is a commonly diagnosed cancer in men. The ethanolic extract of propolis (EEP) and its phenolic compounds possess immunomodulatory, chemopreventive and antitumor effects. Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL/APO2L) is a naturally occurring anticancer agent that preferentially induces apoptosis in cancer cells and is not toxic to normal cells. We examined the cytotoxic and apoptotic effects of EEP and phenolic compounds isolated from propolis in combination with TRAIL on two prostate cancer cell lines, hormone-sensitivity LNCaP and hormone-refractory DU145. The cytotoxicity was evaluated by MTT and LDH assays. The apoptosis was determined using flow cytometry with annexin V-FITC/propidium iodide. The prostate cancer cell lines were proved to be resistant to TRAIL-induced apoptosis. Our study demonstrated that EEP and its components significantly sensitize to TRAIL-induced death in prostate cancer cells. The percentage of the apoptotic cells after cotreatment with 50 μg mL−1EEP and 100 ng mL−1TRAIL increased to 74.9 ± 0.7% for LNCaP and 57.4 ± 0.7% for DU145 cells. The strongest cytotoxic effect on LNCaP cells was exhibited by apigenin, kaempferid, galangin and caffeic acid phenylethyl ester (CAPE) in combination with TRAIL (53.51 ± 0.68–66.06 ± 0.62% death cells). In this work, we showed that EEP markedly augmented TRAIL-mediated apoptosis in prostate cancer cells and suggested the significant role of propolis in chemoprevention of prostate cancer.

scholarly journals Identifying metastatic ability of prostate cancer cell lines using native fluorescence spectroscopy and machine learning methods

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Jianpeng Xue ◽  
Yang Pu ◽  
Jason Smith ◽  
Xin Gao ◽  
Chun Wang ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Machine Learning ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Prostate Cancer Cell ◽  
Cancer Cell Lines ◽  
Prostate Cancer Cells ◽  
Prostate Cancer Cell Lines ◽  
Native Fluorescence

AbstractMetastasis is the leading cause of mortalities in cancer patients due to the spreading of cancer cells to various organs. Detecting cancer and identifying its metastatic potential at the early stage is important. This may be achieved based on the quantification of the key biomolecular components within tissues and cells using recent optical spectroscopic techniques. The aim of this study was to develop a noninvasive label-free optical biopsy technique to retrieve the characteristic molecular information for detecting different metastatic potentials of prostate cancer cells. Herein we report using native fluorescence (NFL) spectroscopy along with machine learning (ML) to differentiate prostate cancer cells with different metastatic abilities. The ML algorithms including principal component analysis (PCA) and nonnegative matrix factorization (NMF) were used for dimension reduction and feature detection. The characteristic component spectra were used to identify the key biomolecules that are correlated with metastatic potentials. The relative concentrations of the molecular spectral components were retrieved and used to classify the cancer cells with different metastatic potentials. A multi-class classification was performed using support vector machines (SVMs). The NFL spectral data were collected from three prostate cancer cell lines with different levels of metastatic potentials. The key biomolecules in the prostate cancer cells were identified to be tryptophan, reduced nicotinamide adenine dinucleotide (NADH) and hypothetically lactate as well. The cancer cells with different metastatic potentials were classified with high accuracy using the relative concentrations of the key molecular components. The results suggest that the changes in the relative concentrations of these key fluorophores retrieved from NFL spectra may present potential criteria for detecting prostate cancer cells of different metastatic abilities.

scholarly journals The impact of Icariside II on human prostate cancer cell proliferation, mobility, and autophagy via PI3K-AKT-mTOR signaling pathway

2020 ◽  
Author(s):  
Shuang Li ◽  
Yunlu Zhan ◽  
Yingwei Xie ◽  
Yonghui Wang ◽  
Yuexin Liu
Keyword(s):  
Prostate Cancer ◽  
Cell Cycle ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Prostate Cancer Cell ◽  
Human Prostate ◽  
Human Prostate Cancer ◽  
Prostate Cancer Cells ◽  
The Impact

Abstract Background The flavonol glycoside icariside Ⅱ (ICA II) has been shown to exhibit a range of anti-tumor properties. Herein we evaluated the impact of ICA II on the proliferation, motility, and autophagy activity of human prostate cancer cells, and we further evaluated the molecular mechanisms underlying these effects. Methods Herein, we treated DU145 human prostate cancer cells with a range of ICA II doses. We then evaluated the proliferative abilities of these cells via CCK-8 assay, whereas apoptosis and cell cycle status were assessed via flow cytometry. We further utilized wound healing and transwell assays to probe the impact of ICA II on migratory and invasive activities, while autophagy was assessed via laser confocal fluorescence microscopy. Western blotting was further utilized to measure LC3-II/I, Beclin-1, P70S6K, PI3K, AKT, mTOR, phospho-AKT, phospho-mTOR, and phospho-P70S6K levels, with RT-PCR being used to evaluate the expression of these same genes at the mRNA level. Results We found that ICA II was capable of mediating a dose- and time-dependent suppression of prostate cancer cell proliferative activity, while also causing these cells to enter a state of cell cycle arrest and apoptosis. We further determined that ICA II treatment was associated with significant impairment of prostate cancer cell migratory and invasive abilities, whereas autophagy was enhanced in treated cells relative to untreated controls. Levels of p-P70S6K, p-mTOR, p-AKT, and PI3K were all also decreased by ICA II. Conclusion Our results indicate that ICA II treatment is capable of suppressing human prostate tumor cell proliferation and disrupting migratory activity while enhancing autophagy through PI3K-AKT-mTOR signaling. As such, ICA II may be an ideal candidate drug for the treatment of prostate cancer.

scholarly journals Expression and action of the growth hormone releasing peptide ghrelin and its receptor in prostate cancer cell lines

2002 ◽  
Vol 172 (3) ◽  
pp. R7-11 ◽  
Author(s):  
PL Jeffery ◽  
AC Herington ◽  
LK Chopin
Keyword(s):  
Prostate Cancer ◽  
Growth Hormone ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Prostate Cancer Cell ◽  
Cancer Cell Lines ◽  
Prostate Cancer Cells ◽  
Normal Prostate ◽  
Prostate Cancer Cell Lines

This study has examined the expression of two new facets of the growth hormone axis, the growth hormone secretagogue receptor (GHS-R) and its recently identified putative natural ligand ghrelin, in prostate cancer cells. GHS-R 1a and 1b isoforms and ghrelin mRNA expression were detected by RT-PCR in the ALVA-41, LNCaP, DU145 and PC3 prostate cancer cell lines. A normal prostate cDNA library expressed GHS-R1a, but not the 1b isoform or ghrelin. Immunohistochemical staining for the GHS-R 1a isoform and ghrelin was positive in the four cell lines studied. PC3 cells showed increased cell proliferation in vitro in response to ghrelin to levels 33% above untreated controls, implying a potential tumour-promoting role for ghrelin in this tissue. This study is the first to demonstrate the co-expression of the GHS-R and ghrelin in prostate cancer cells. It is also the first study to provide evidence that a previously unrecognised autocrine/paracrine pathway involving ghrelin, that is capable of stimulating growth, exists in prostate cancer.

scholarly journals SOX4 induces tumor invasion by targeting EMT-related pathway in prostate cancer

Tumor Biology ◽  
2017 ◽  
Vol 39 (5) ◽  
pp. 101042831769453 ◽  
Author(s):  
Yifan Liu ◽  
Shan Zeng ◽  
Xianhan Jiang ◽  
Dehui Lai ◽  
Zhengming Su
Keyword(s):  
Prostate Cancer ◽  
Cell Proliferation ◽  
Cell Lines ◽  
Cancer Cell ◽  
Prostate Cancer Cell ◽  
Epithelial Mesenchymal Transition ◽  
Cancer Cell Lines ◽  
Prostate Cancer Cell Lines ◽  
Mesenchymal Transition ◽  
Cancer Tissues

SOX4 (sex-determining region Y-related high-mobility group box 4) is associated with tumor progression and poor clinical outcome in several cancers. This study aims to evaluate whether SOX4 affects the biological behaviors of prostate cancer and further elucidate whether this effect works through the epithelial–mesenchymal transition pathway. We investigated the expression of SOX4 in a series of prostate cancer tissues and adjacent noncancerous tissues, as well as in a panel of prostate cancer cell lines. Cell proliferation, migration, and invasion were evaluated in SOX4 knockdown prostate cancer cell lines by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and Transwell assay. Our results showed that the expression of SOX4 was remarkably upregulated both in prostate cancer tissues and in cell lines. Knockdown of SOX4 repressed the ability of cell proliferation and migration of DU145 cells. Moreover, inhibition of SOX4 could reverse the epithelial–mesenchymal transition processes through upregulation of E-cadherin and downregulation of vimentin. This study provided evidence that SOX4 could serve as a potential therapeutic target in prostate cancer.

Attomolar detection of extracellular microRNAs released from living prostate cancer cells by a plasmonic nanowire interstice sensor

Nanoscale ◽  
2017 ◽  
Vol 9 (44) ◽  
pp. 17387-17395 ◽  
Author(s):  
Siyeong Yang ◽  
Hongki Kim ◽  
Kyung Jin Lee ◽  
Seul Gee Hwang ◽  
Eun-Kyung Lim ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Prostate Cancer Cell ◽  
Human Prostate ◽  
Human Prostate Cancer ◽  
Prostate Cancer Cells ◽  
Human Prostate Cancer Cell ◽  
Prostate Cancer Cell Lines

Extracellular miR141 and miR375 released from living human prostate cancer cell lines were clearly verified by using an extremely sensitive and specific PNI sensor.

scholarly journals 1α,25-Dihydroxyvitamin D3 Reduces c-Myc Expression, Inhibiting Proliferation and Causing G1 Accumulation in C4-2 Prostate Cancer Cells

Endocrinology ◽  
2009 ◽  
Vol 150 (5) ◽  
pp. 2046-2054 ◽  
Author(s):  
JoyAnn N. Phillips Rohan ◽  
Nancy L. Weigel
Keyword(s):  
Prostate Cancer ◽  
Vitamin D ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Prostate Cancer Cell ◽  
Glycogen Synthase ◽  
Mrna Levels ◽  
Prostate Cancer Cells ◽  
Dihydroxyvitamin D3

There is an inverse correlation between exposure to sunlight (the major source of vitamin D) and the risk for prostate cancer, the most common noncutaneous cancer and second most common cause of death from cancer in American men. The active metabolite of vitamin D, 1α,25-dihydroxyvitamin D3 [1,25(OH)2D3] acting through the vitamin D receptor decreases prostate cancer cell growth and invasiveness. The precise mechanisms by which 1,25(OH)2D3 inhibits growth in prostate cancer have not been fully elucidated. Treatment with 1,25(OH)2D3 causes an accumulation in the G0/G1 phase of the cell cycle in several prostate cancer cell lines. One potential target known to regulate the G0/G1 to S phase transition is c-Myc, a transcription factor whose overexpression is associated with a number of cancers including prostate cancer. We find that 1,25(OH)2D3 reduces c-Myc expression in multiple prostate epithelial cell lines, including C4-2 cells, an androgen-independent prostate cancer cell line. Reducing c-Myc expression to the levels observed after 1,25(OH)2D3 treatment resulted in a comparable decrease in proliferation and G1 accumulation demonstrating that down-regulation of c-Myc is a major component in the growth-inhibitory actions of 1,25(OH)2D3. Treatment with 1,25(OH)2D3 resulted in a 50% decrease in c-Myc mRNA but a much more extensive reduction in c-Myc protein. Treatment with 1,25(OH)2D3 decreased c-Myc stability by increasing the proportion of c-Myc phosphorylated on T58, a glycogen synthase kinase-3β site that serves as a signal for ubiquitin-mediated proteolysis. Thus, 1,25(OH)2D3 reduces both c-Myc mRNA levels and c-Myc protein stability to inhibit growth of prostate cancer cells.

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