Methylation of Integrin α4 and E-Cadherin Genes in Human Prostate Cancer

Mostafavi‐Pour, Zohreh; Kianpour, Sedigheh; Dehghani, Mehdi; Mokarram, Pooneh; Torabinejad, Simin; Monabati, Ahmad

doi:10.1007/s12253-015-9917-8

Cited by 16 publications

(13 citation statements)

References 37 publications

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“…MTT‐assay was done for cytotoxicity analysis of the obtained nanoparticles on Hep‐G2 cell line in 96‐well plates at a density of 1 × 10 4 cells/well in a humidified 5% CO 2 incubator at 37°C. After 24 h of incubation, the prepared culture by RPMI 1640 media was replaced by 100 µL of media with different concentrations of the nanoparticles (4,000, 1,000, 500, 100, 50, 5, and 1 µg/mL) . Then, the cells were incubated for a period of 24 and 48 h. After completion of the exposure time, the media was carefully removed and replaced with 25 µL of MTT [3‐(4, 5‐dimethylthiazol‐2‐yl)‐2, 5‐diphenyltetrazolium bromide] solution for 3 h. Then, 100 µL of DMSO was added to each well, and the absorbance was measured at 540 nm using a microplate spectrophotometer (Power wave X52, BioTek instrument Inc., USA).…”

Section: Methodsmentioning

confidence: 99%

Characterization of biogenic Fe (III)‐binding exopolysaccharide nanoparticles produced by Ralstonia sp. SK03

Kianpour

Ebrahiminezhad

Negahdaripour

et al. 2018

Biotechnology Progress

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A new technological approach to nanoparticle synthesis is using microorganisms, such as bacteria, which have the ability to synthesize nontoxic nanoparticles with high biocompatibility. In addition, bacteria have strict control over size, structure, shape, and dimension of produced nanoparticles. In the present work, Fe (III)-binding exopolysaccharide (Fe-EPS) nanoparticles were biosynthesized by Ralstonia pickettii sp. SK03, a bacterium isolated from a mineral spring. 16S rRNA gene sequencing and biochemical tests were done for identification of the isolated bacterium. For the first time, critical biological and physicochemical properties of this iron oxide nanoparticle were characterized using Fourier Transform Infrared (FTIR) Spectroscopy, Transmission Electron Microscopy (TEM), Vibrating Sample Magnetometer (VSM), Dynamic Light Scattering (DLS), Thermogravimetric analysis (TGA), X-ray crystallography (XRD), Atomic absorption spectroscopy (AAS), and cell viability assays (MTT assay). The characterization results showed that Fe-EPS nanoparticles were composed of spherical ferrihydrite nanoparticles (with a size range of 1.2-2 nm), trapped in a polysaccharide matrix. The TGA analysis demonstrated that Fe-EPS nanoparticles contained ∼25.2% polysaccharide. Therefore, this polysaccharide matrix showed a very low magnetic saturation value (0.25 emu/g) and a large negative charge of -93.8 mV. In addition, treatment of hepatocarcinoma cell line (Hep-G2) with 1-500 µg/mL concentrations of Fe-EPS nanoparticles caused 40% increase in the cell viability, which indicated that the biosynthesized nanoparticles were nontoxic and biocompatible. © 2018 American Institute of Chemical Engineers Biotechnol. Prog., 2018 © 2018 American Institute of Chemical Engineers Biotechnol. Prog., 34:1167-1176, 2018.

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Section: Methodsmentioning

confidence: 99%

Characterization of biogenic Fe (III)‐binding exopolysaccharide nanoparticles produced by Ralstonia sp. SK03

Kianpour

Ebrahiminezhad

Negahdaripour

et al. 2018

Biotechnology Progress

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“…Downregulation of E-cadherin results in increased invasiveness of distinct types of cancer, such as gastric (65,66), breast (67), ovary (68,69), endometrial (70), thyroid (71), hepatocellular carcinoma (72), oral (73), and pancreatic (74), and has been well documented in prostate adenocarcinoma (75)(76)(77). In PC, E-cadherin expression has been shown to be reduced by activation of AKT signaling (78), by high expression of transcription factors such as Snail (79,80), Slug (81), Twist (82) and WT1 (48), and by hypermethylation of the E-cadherin promoter (83). The loss of this important cell adhesion molecule is a critical early event in invasion and metastasis that leads to the conversion from a stationary to a migratory cell phenotype (84).…”

Section: Wt1 Suppression Of E-cadherin Promotes Cell Motilitymentioning

confidence: 99%

Functional Role of WT1 in Prostate Cancer

et al. 2016

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Licence: This open access article is licensed under Creative Commons Attribution 4.0 International (CC BY 4.0). http://creativecommons.org/licenses/by/4.0/ Users are allowed to share (copy and redistribute the material in any medium or format) and adapt (remix, transform, and build upon the material for any purpose, even commercially), as long as the authors and the publisher are explicitly identified and properly acknowledged as the original source. AbstractAlthough initial discoveries of Wilms tumor 1 (WT1) expression in extrarenal disease generated controversy, we and others have examined WT1 expression in non-Wilms cancers and have demonstrated that the WT1(A) isoform, lacking the lysine-threonine-serine tripeptide (KTS) insertion, transcriptionally regulates the expression of growth control genes in other cancer types. Here, we review our evidence that WT1 is expressed in prostate cancer (PC) epithelial cells and regulates PC critical genes. That WT1 may promote metastatic disease is consistent with previous findings that WT1 suppressed E-cadherin and enhanced motility of PC cells with low migratory and metastatic potential. Recent findings led us to askFraizer et al. 236whether WT1 acts as an angiogenic switch in PC. Although vascular endothelial growth factor (VEGF) is regulated at several levels and by a number of different factors, a mechanistic understanding of WT1-mediated transcriptional regulation in PC cells was previously lacking. Here, we discuss the evidence of WT1-and androgen receptor (AR)-binding sites in the VEGF promoter and show the potential for cooperation between hormone and WT1. These findings revealed that in AR-intact PC cells, WT1 was sufficient to upregulate VEGF transcription, and WT1 expression enhanced the hormone activation of VEGF expression. This notion that WT1 can activate an angiogenic switch in PC cells, to enhance tumor growth and progression to metastatic disease, is consistent with our understanding of the oncogenic nature of WT1 overexpression in inappropriate tissues or at inappropriate times. The potential for WT1 to promote both tumor angiogenesis and PC cell migration suggests that WT1 regulates genes that promote PC progression to lethal metastatic disease. Therapies targeting WT1 in PC may reduce metastatic spread and increase overall survival.

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“…Different mechanisms have been implicated with E-cadherin downregulation in human medicine, including copy number loss (Saramaki and Visakorpi, 2007), somatic mutations (Busch et al, 2017), methylation (Graff et al, 1995; Yoshiura et al, 1995; Li et al, 2001; Mostafavi-Pour et al, 2015), and suppression mediated by ZEB1 and SRC family kinases (Mostafavi-Pour et al, 2015). CDH1 gene repression promoted by its promoter hypermethylation, plays a crucial role in tumor invasion and spread (Graff et al, 1995; Yoshiura et al, 1995; Li et al, 2001; Mostafavi-Pour et al, 2015). CDH1 hypermethylation and E-cadherin downregulation have been reported in more than 75% of patients with metastatic PC (Maruyama et al, 2002; Singal et al, 2004; Hoque et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

“…CDH1 hypermethylation and E-cadherin downregulation have been reported in more than 75% of patients with metastatic PC (Maruyama et al, 2002; Singal et al, 2004; Hoque et al, 2005). Also, CDH1 promoter methylation is widely studied as a cause of E-cadherin down-regulation in human PC (Graff et al, 1995; Yoshiura et al, 1995; Li et al, 2001; Mostafavi-Pour et al, 2015). However, conflicting results have been reported due to the difficulties in studying methylation (Zhang et al, 2016b).…”

Section: Introductionmentioning

confidence: 99%

E-Cadherin Downregulation is Mediated by Promoter Methylation in Canine Prostate Cancer

et al. 2019

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E-cadherin is a transmembrane glycoprotein responsible for cell-to-cell adhesion, and its loss has been associated with metastasis development. Although E-cadherin downregulation was previously reported in canine prostate cancer (PC), the mechanism involved in this process is unclear. It is well established that dogs, besides humans, spontaneously develop PC with high frequency; therefore, canine PC is an interesting model to study human PC. In human PC, CDH1 methylation has been associated with E-cadherin downregulation. However, no previous studies have described the methylation pattern of CDH1 promoter in canine PC. Herein, we evaluated the E-cadherin protein and gene expression in canine PC compared to normal tissues. DNA methylation pattern was investigated as a regulatory mechanism of CDH1 silencing. Our cohort is composed of 20 normal prostates, 20 proliferative inflammatory atrophy (PIA) lesions, 20 PC, and 11 metastases from 60 dogs. The E-cadherin protein expression was assessed by immunohistochemistry and western blotting and gene expression by qPCR. Bisulfite- pyrosequencing assay was performed to investigate the CDH1 promoter methylation pattern. Membranous E-cadherin expression was observed in all prostatic tissues. A higher number of E-cadherin negative cells was detected more frequently in PC compared to normal and PIA samples. High-grade PC showed a diffuse membranous positive immunostaining. Furthermore, PC patients with a higher number of E-cadherin negative cells presented shorter survival time and higher Gleason scores. Western blotting and qPCR assays confirmed the immunohistochemical results, showing lower E-cadherin protein and gene expression levels in PC compared to normal samples. We identified CDH1 promoter hypermethylation in PIA and PC samples. An in vitro assay with two canine prostate cancer cells (PC1 and PC2 cell lines) was performed to confirm the methylation as a regulatory mechanism of E-cadherin expression. PC1 cell line presented CDH1 hypermethylation and after 5-Aza-dC treatment, a decreased CDH1 methylation and increased gene expression levels were observed. Positive E-cadherin cells were massively found in metastases (mean of 90.6%). In conclusion, low levels of E-cadherin protein, gene downregulation and CDH1 hypermethylation was detected in canine PC. However, in metastatic foci occur E-cadherin re-expression confirming its relevance in these processes.

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Methylation of Integrin α4 and E-Cadherin Genes in Human Prostate Cancer

Cited by 16 publications

References 37 publications

Characterization of biogenic Fe (III)‐binding exopolysaccharide nanoparticles produced by Ralstonia sp. SK03

Characterization of biogenic Fe (III)‐binding exopolysaccharide nanoparticles produced by Ralstonia sp. SK03

Functional Role of WT1 in Prostate Cancer

E-Cadherin Downregulation is Mediated by Promoter Methylation in Canine Prostate Cancer

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