Role of MicroRNA-101 on Proliferation and Migration of Prostate Cancer Cells

2021 ◽  
Vol 11 (10) ◽  
pp. 2076-2080
Author(s):  
Yiming Weng ◽  
Jun Xiang ◽  
Wei Le ◽  
Yuanshen Mao
Keyword(s):  
Prostate Cancer ◽  
Control Groups ◽  
Cancer Pathogenesis ◽  
Pc3 Cells ◽  
Cox 2 ◽  
And Migration ◽  
And Control ◽  
Mtt Assays ◽  
Proliferation And Migration

Background: MicroRNA-101 is a tumor inhibitor that stimulates tumor progression by reducing or inhibiting the expression of certain oncogenes. Some studies presented that cox-2 is target of MicroRNA 101 in prostate cancer process. Methods: MicroRNA-101 expression was detected by RT-PCR in PC3 cell lines. A and to determine cell proliferation we used MTT assays. Cell would heal and Flow cytometry assays were also used to detect cellular migratory ability and apoptosis, respectively. To assess cox-2 protein expression, Immunohistochemistry was used and data analyzed by data analysis by SPSS 20. Results: PC3 cells treated by MicroRNA-101 mimics displayed a 24% elevation in growth rate compared with blank (P < 0.01) at 48 h, and a 12% increase (P < 0.01) at 72 h. On the other hand, at 48 and 72 h after the MicroRNA-101 inhibitor transfection, proliferation of PC3 cell was decreased significantly. The early apoptosis rate in transfected PC3 cells with MicroRNA-101 mimic (74.4%) and inhibitor (22.8%) were significantly different at 72 h after transfection (P < 0.05), MicroRNA-101 mimics inhibited cell migration, adhesion, and spread was wider relative to the group of control and inhibitor for the PC3 cells. Expression of Cox-2 in transfected PC3 with the MicroRNA-101 inhibitor was higher than the mimic and control groups significantly (P < 0.01). Conclusion: MicroRNA-101 by Cox-2 can play key roles in the prostate cancer pathogenesis.

scholarly journals Moringa oleifera Alkaloids Inhibited PC3 Cells Growth and Migration Through the COX-2 Mediated Wnt/β-Catenin Signaling Pathway

2020 ◽  
Vol 11 ◽  
Author(s):  
Jing Xie ◽  
Feng-xian Luo ◽  
Chong-ying Shi ◽  
Wei-wei Jiang ◽  
Ying-yan Qian ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Cycle ◽  
Moringa Oleifera ◽  
Prostate Cancer Cells ◽  
Cycle Arrest ◽  
Pc3 Cells ◽  
Cox 2 ◽  
And Migration ◽  
Proliferation And Migration

Moringa oleifera Lam. (M. oleifera) is valuable plant distributed in many tropical and subtropical countries. It has a number of medicinal uses and is highly nutritious. M. oleifera has been shown to inhibit tumor cell growth, but this effect has not been demonstrated on prostate cancer cells. In this study, we evaluated the inhibitory effect of M. oleifera alkaloids (MOA) on proliferation and migration of PC3 human prostate cancer cells in vitro and in vivo. Furthermore, we elucidated the mechanism of these effects. The results showed that MOA inhibited proliferation of PC3 cells and induced apoptosis and cell cycle arrest. Furthermore, MOA suppressed PC3 cell migration and inhibited the expression of matrix metalloproteinases (MMP)-9. In addition, MOA significantly downregulated the expression of cyclooxygenase 2 (COX-2), β-catenin, phosphorylated glycogen synthase 3β, and vascular endothelial growth factor, and suppressed production of prostaglandin E2 (PGE2). Furthermore, FH535 (β-catenin inhibitor) and MOA reversed PGE2-induced PC3 cell proliferation and migration, and the effects of MOA and FH535 were not additive. In vivo experiments showed that MOA (150 mg/kg) significantly inhibited growth of xenograft tumors in mice, and significantly reduced the protein expression levels of COX-2 and β-catenin in tumor tissues. These results indicate that MOA inhibits the proliferation and migration, and induces apoptosis and cell cycle arrest of PC3 cells. Additionally, MOA inhibits the proliferation and migration of PC3 cells through suppression of the COX-2 mediated Wnt/β-catenin signaling pathway.

A blinded, randomized controlled trial of neo-adjuvant celecoxib in patients with early prostate cancer

2006 ◽  
Vol 24 (18_suppl) ◽  
pp. 4563-4563 ◽  
Author(s):  
P. Sooriakumaran ◽  
P. Macanas-Pirard ◽  
S. Fox ◽  
H. Coley ◽  
G. Bucca ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Prostate Cancer ◽  
Cell Proliferation ◽  
Statistical Significance ◽  
Observer Agreement ◽  
Control Groups ◽  
Ki 67 ◽  
In Vivo Models ◽  
Cox 2 ◽  
And Control

4563 Background: Celecoxib inhibits tumorigenesis in many in vitro and in vivo models by anti-angiogenesis, induction of apoptosis, and inhibition of tumour cell proliferation and hypoxia. Methods: 45 cT1–2 prostate cancer patients were block randomized 2:1 to four weeks celecoxib 400mg b.d. or no drug prior to radical prostatectomy (RP). Tumour immunohistochemistry was performed for cell proliferation (Ki-67), angiogenesis (CD-31, VEGF, VEGF-R2), hypoxia (HIF-1), apoptosis (TUNEL), and COX-2. All scoring was performed blind by PS and a random 20% were validated blindly by an immunopathologist (SBF). In 19 patients (12 celecoxib-treated, 7 control), peri-operative peripheral zone biopsies were subjected to cDNA microarray analysis to identify differences in gene expression profiling (GEP) between the groups. Results: There was ‘substantial’ (kappa >0.6) or ‘almost perfect’ (kappa >0.8) inter-observer agreement in immunoscoring for all stains. Baseline scores were not significantly different between the celecoxib and control groups. In the celecoxib group, RP scores were significantly lower for Ki-67 (p = 0.036), and non-significantly lower for hypoxia (p = 0.15), KDR (p = 0.16), COX-2 (p = 0.19), microvessel density (p = 0.53), and VEGF (p = 0.83); tumour apoptosis was non-significantly higher (p = 0.26). MANOVA of the full model of stains showed that the difference between the two groups approached statistical significance (p = 0.058), and this was visualized with principal component analysis. GEP revealed that 76 genes were significantly differentially expressed between the celecoxib and control groups using uncorrected t-tests. In the celecoxib group, the tumour suppressor gene p73 and genes associated with protection against oxidative stress were significantly up-regulated; genes associated with cell adhesion were significantly down-regulated, consistent with a reduction in metastatic potential. Conclusions: Celecoxib appears to have marked anti-cancer effects on prostate tumours, most notably affecting cell cycle regulation, oxidative stress, and cell signalling. It may therefore be a promising agent in the management of prostate cancer and warrants further investigation. No significant financial relationships to disclose.

scholarly journals Suppression of MicroRNA-144 Promotes CXCR4 and CXCL12 Expression and Downregulates Apoptosis in Ovarian Cancer Cells

2020 ◽  
Author(s):  
Fatma Aysun Turut ◽  
Hilal Acidereli ◽  
Ozge Cevik
Keyword(s):  
Ovarian Cancer ◽  
Cancer Cells ◽  
Ovarian Cancer Cells ◽  
The Novel ◽  
Cxcl12 Expression ◽  
Protein Expressions ◽  
Cox 2 ◽  
And Migration ◽  
Proliferation And Migration

AbstractMicroRNAs are important regulators in the growth and metastasis of ovarian cancers. Many assays were established to identify the role of miR-144-3p in ovarian cancer cells and its interaction with COX-2 and chemokines (CXCR4 and CXCL12). The ovarian cancer cells (OVCAR-3 and SKOV-3) were transfected with Anti-miR-144 to downregulate the miR-144-3p and cultured for 36 h. We herein examined the cell viability, colony formation, cell migration, COX-2 reporter activity, the protein expressions of CXCR4, CXCL12, COX-2, VEGF, Caspase-3, BAX and Bcl-2. We have observed that the suppression of miR-144-3p significantly increased the cell proliferation and migration and decreased the apoptosis. Moreover, the downregulation of miR-144-3p markedly increased the COX-2, CXCR4, CXCL12 and VEGF expression in OVCAR-3 and SKOV-3 ovarian cancer cells. In conclusion, miR-144-3p may play important roles in the regulation of chemokine receptor CXCR4 and its ligand CXCL12 in the progressive ovarian tumors expressing COX2. These data suggests that miR-144 has the novel therapeutic targets for the cancer therapy and cancer prevention.

Role of microenvironment on proliferation and migration of an SDHB silenced murine Pheochromocytoma cell line

2017 ◽  
Author(s):  
Serena Martinelli ◽  
Vanessa D'Antongiovanni ◽  
Susan Richter ◽  
Letizia Canu ◽  
Tonino Ercolino ◽  
...  
Keyword(s):  
Cell Line ◽  
Pheochromocytoma Cell ◽  
And Migration ◽  
Proliferation And Migration

Exosomal miR-214-5p Released from Glioblastoma Cells Modulates Inflammatory Response of Microglia after Lipopolysaccharide Stimulation through Targeting CXCR5

2019 ◽  
Vol 18 (1) ◽  
pp. 78-87 ◽  
Author(s):  
Jian-kai Yang ◽  
Hong-jiang Liu ◽  
Yuanyu Wang ◽  
Chen Li ◽  
Ji-peng Yang ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Critical Role ◽  
Luciferase Reporter ◽  
Clinical Prognosis ◽  
Direct Target ◽  
And Migration ◽  
High Level ◽  
Cxcr5 Expression ◽  
Proliferation And Migration

Background and Objective: Exosomes communicate inter-cellularly and miRNAs play critical roles in this scenario. MiR-214-5p was implicated in multiple tumors with diverse functions uncovered. However, whether miR-214-5p is mechanistically involved in glioblastoma, especially via exosomal pathway, is still elusive. Here we sought to comprehensively address the critical role of exosomal miR-214-5p in glioblastoma (GBM) microenvironment.Methods:The relative expression of miR-214-5p was determined by real-time PCR. Cell viability and migration were measured by MTT and transwell chamber assays, respectively. The secretory cytokines were measured with ELISA kits. The regulatory effect of miR-214-5p on CXCR5 expression was interrogated by luciferase reporter assay. Protein level was analyzed by Western blot.Results:We demonstrated that miR-214-5p was aberrantly overexpressed in GBM and associated with poorer clinical prognosis. High level of miR-214-5p significantly contributed to cell proliferation and migration. GBM-derived exosomal miR-214-5p promoted inflammatory response in primary microglia upon lipopolysaccharide challenge. We further identified CXCR5 as the direct target of miR-214- 5p in this setting.Conclusion:Overexpression of miR-214-5p in GBM modulated the inflammatory response in microglia via exosomal transfer.

scholarly journals DIAPH2, PTPRD and HIC1 Gene Polymorphisms and Laryngeal Cancer Risk

2021 ◽  
Vol 18 (14) ◽  
pp. 7486
Author(s):  
Mirosław Śnit ◽  
Maciej Misiołek ◽  
Wojciech Ścierski ◽  
Anna Koniewska ◽  
Grażyna Stryjewska-Makuch ◽  
...  
Keyword(s):  
Cancer Risk ◽  
Laryngeal Cancer ◽  
Basic Research ◽  
Control Groups ◽  
Allele Distribution ◽  
Study Results ◽  
Risk Patients ◽  
And Control ◽  
The Relationship

AIM, DIAPH2, PTPRD and HIC1 are the cell glycoprotein, which play an important role in the occurrence and development of tumors. This study was designed to assess the association between DIAPH2, PTPRD and HIC1 SNPs and laryngeal cancer risk. PATIENTS AND METHODS: This study including 267 patients with histologically confirmed laryngeal cancer and 157 controls. The relationship between genetic variations DIAPH2 (rs6620138), PTPRD (rs3765142) and HIC1 (rs9901806) and the onset of laryngeal cancer were investigated. Statistical analysis to calculate the relationship between DIAPH2, PTPRD and HIC1 genes polymorphism and pathogenesis of laryngeal cancer. RESULTS: The results showed that rs6620138 DIAPH2 polymorphism could increase the onset risk of laryngeal cancer. Statistically significant differences in allele distribution of rs6620138 DIAPH2 and rs9901806 HIC1 in the case and control groups subgroups. CONCLUSIONS: This study results suggested that genetic variation of rs6620138 DIAPH2 polymorphism is related to the susceptibility to laryngeal cancer. Our results provide a basis to begin basic research on the role of DIAPH2 gene in the pathogenesis of laryngeal cancer.

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