Tumor necrosis factor-α-induced a disintegrin and metalloprotease 10 increases apoptosis resistance in prostate cancer cells

Zhu, Lijia; Zhao, Sheng; Xu, Ting; Wang, He

doi:10.3892/ol.2014.1810

Cited by 11 publications

(8 citation statements)

References 36 publications

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“…Prostate cancer (PCa) continues to plague males worldwide, ranking as a leading contributor of male death particularly in developed countries [1,2]. In China, PCa has exhibited a progressively increasing incidence and mortality rate, with a relatively higher incidence identified in urban regions and greater mortality in rural areas [3].…”

Section: Introductionmentioning

confidence: 99%

RETRACTED ARTICLE: The involvement of FBP1 in prostate cancer cell epithelial mesenchymal transition, invasion and metastasis by regulating the MAPK signaling pathway

et al. 2019

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Prostate cancer (PCa) is a frequently occurring malignancy in males, and epithelial mesenchymal transition (EMT) plays a critical role in PCa metastasis. Thus, developing biomarkers inhibiting EMT may provide significance for treatment of PCa. Hence, the aim of the current study was to investigate the mechanism by which FBP1 gene silencing influences PCa cell EMT, invasion and metastasis by mediating the MAPK pathway. PCa cell lines exhibiting the highest FBP1 expression were selected and treated with plasmids of siRNA-FBP1 sequence 1 and 2, pcDNA3.1-Flag-FBP1 (over-expression plasmid of FBP1), U0126 (an inhibitor of the ERK signaling pathway) and PD98059 (an inhibitor of the MEK signaling pathway). Cell proliferation, migration and invasion were detected by MTT assay, wound healing assay and Transwell assay, respectively. The mRNA and protein expression of related factors of EMT and MAPK signaling were determined by RT-qPCR and western blot analysis, respectively. Xenograft tumor growth after inoculation of DU145 cells was regularly analyzed in the nude mice. The positive expression of EMT markers was determined by immunohistochemistry. DU-145 and PC-3 cells displaying the highest FBP1 expression were selected for further analysis. The PCa cells treated with siRNA-FBP1 exhibited increased proliferation, migration rate and invasion, in addition to facilitated xenograft tumor growth. Notably, siRNA-FBP1 was identified to accelerate PCa cell EMT by elevating the expression of Vimentin and N-cadherin while diminishing E-cadherin expression via activation of the MAPK signaling pathway. The aforementioned results were reversed in PCa cells treated by pcDNA3.1-Flag-FBP1. Evidence has been provided in this study that FBP1 gene silencing activates the MAPK pathway, which ultimately promotes cell EMT, invasion and metastasis in PCa.

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Section: Introductionmentioning

confidence: 99%

RETRACTED ARTICLE: The involvement of FBP1 in prostate cancer cell epithelial mesenchymal transition, invasion and metastasis by regulating the MAPK signaling pathway

et al. 2019

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“…17 Latest reports have shown that ADAM10 siRNA-based gene therapy can be potentially utilized for treatment of different tumors, including prostate cancer. 18…”

Section: Introductionmentioning

confidence: 99%

Functionally modified magnetic nanoparticles for effective siRNA delivery to prostate cancer cells in vitro

et al. 2019

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Different types of siRNA delivery vehicles including nanoparticles have been synthesized and utilized for prostate cancer gene therapy. However, one of the most common limitations being faced is the toxicity of cationic polymers toward the cells. In the current study, magnetic nanoparticles were prepared and conjugated with cationic polymer, polyethylenimine. Then polyethylene glycol was conjugated with polyethylenimine to improve the biocompatibility of nanoparticles. The transmission electron microscopy size of nanoparticles was found to be 15.82 (±9.07) nm, while hydrodynamic size was about 79.20 (±0.68) nm. Zeta potential analysis of polyethylenimine and polyethylene glycol-coated nanoparticles was +31.4 (±0.62) and +5.65 (±0.76) mV, respectively. Fourier transform infrared spectroscopy and 1H nuclear magnetic resonance confirmed the presence of polyethylene glycol and polyethylenimine polymers in magnetic nanoparticles. Cell viability test in mouse fibroblast NIH 3T3 and prostate cancer PC3 cells showed an increased in biocompatibility of functionally modified polyethylene glycol–polyethylenimine–Fe3O4 nanoparticles. siRNA targeting a disintegrin and metalloproteinase 10 (ADAM10) was successfully loaded into the polyethylene glycol–polyethylenimine–Fe3O4 nanoparticles and delivered to PC3 cells. The results clearly demonstrated a significant decrease in cell viability, which increased within a certain siRNA concentration. The inhibitory concentration (IC50) value for ADAM10 siRNA was calculated to be 15.83 nM after 72 h. Confocal microscopy confirmed the delivery of siRNA-loaded nanoparticles intracellularly to the tumor cells cytosol. This magnetic system can be used as a powerful platform to inhibit cancer cells progression.

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“…To date, increasing evidence has demonstrated that ADAM10 affects the production of the inflammatory cytokines IL-6 and IL-1β in macrophages and thus, is implicated in the process of leukocyte migration and in the promotion of pro-inflammatory activity [ 18 - 20 ]. Some studies have revealed that ADAM10 inhibitors performed beneficial functions, such as increasing apoptosis resistance or suppressing the inflammatory immune response, in several cell models [ 21 - 23 ]. This evidence suggests that ADAM10 may play a vital role in the pathogenesis of directly inflammatory-related diseases, such as sepsis.…”

Section: Introductionmentioning

confidence: 99%

An ADAM10 promoter polymorphism is a functional variant in severe sepsis patients and confers susceptibility to the development of sepsis

et al. 2015

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IntroductionAlthough genetic variants of the A disintegrin and metalloproteinase 10 (ADAM10) gene have been shown to be associated with susceptibility to several inflammatory-related diseases, to date little is known about the clinical relationship in the development of sepsis.MethodsTwo genetic variants in the promoter of ADAM10 were selected to analyze the potential association with the risk of sepsis. A total of 440 sepsis patients and 450 matched healthy individuals in two independent Chinese Han population were enrolled. Pyrosequencing and polymerase chain reaction-length polymorphism was used to determine the genotypes of the rs514049 and rs653765. A real-time qPCR method was used to detect the mRNA level of ADAM10. Enzyme-linked immunosorbent assay was used to measure the expression levels of substrates CX3CL1, interleukin (IL)-6R, tumor necrosis factor alpha (TNF-α), and the pro-inflammatory cytokines IL-1β and IL-6. Luciferase assay was used to analyze the activities of the promoter haplotypes of ADAM10.ResultsNo statistically significant differences between sepsis cases and controls in the genotype or allele frequencies were observed, suggesting that ADAM10 single nucleotide polymorphisms (SNPs) may not be risk factors for the occurrence of sepsis. A significant difference in the genotype and allele frequencies of the rs653765 SNP between patients with sepsis subtype and severe sepsis (P = 0.0014) or severe sepsis/sepsis shock (P = 0.0037) were observed. Moreover, the rs653765 CC genotype in severe sepsis showed a higher ADAM10 level compared to healthy groups, and the rs653765 CC polymorphism had a strong impact on the production of the ADAM10 substrates CX3CL1, IL-6R and TNF-α. Furthermore, the functional assay showed that ADAM10 C-A haplotype carriers exhibited significantly higher reporter activity compared with the T-A carriers and T-C carriers in human acute monocytic leukemia cell line.ConclusionsOur data initially indicated the ADAM10 rs653765 polymorphism was associated with the development of severe sepsis; the risk CC genotype could functionally affect the expression level of ADAM10 mRNA and was accompanied by the up-regulation of its substrates. Thus, ADAM10 might be clinically important and play a critical role in the pathogenesis of the development of sepsis, with potentially important therapeutic implications.Electronic supplementary materialThe online version of this article (doi:10.1186/s13054-015-0796-x) contains supplementary material, which is available to authorized users.

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Tumor necrosis factor-α-induced a disintegrin and metalloprotease 10 increases apoptosis resistance in prostate cancer cells

Cited by 11 publications

References 36 publications

RETRACTED ARTICLE: The involvement of FBP1 in prostate cancer cell epithelial mesenchymal transition, invasion and metastasis by regulating the MAPK signaling pathway

RETRACTED ARTICLE: The involvement of FBP1 in prostate cancer cell epithelial mesenchymal transition, invasion and metastasis by regulating the MAPK signaling pathway

Functionally modified magnetic nanoparticles for effective siRNA delivery to prostate cancer cells in vitro

An ADAM10 promoter polymorphism is a functional variant in severe sepsis patients and confers susceptibility to the development of sepsis

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