Angiotensin II promotes endometrial cancer cell survival

Nowakowska, Magdalena; Matysiak-Burzyńska, Zuzanna Elżbieta; Kowalska, Karolina; Płuciennik, Elżbieta; Domińska, Kamila; Piastowska-Ciesielska, Agnieszka Wanda

doi:10.3892/or.2016.4887

Cited by 15 publications

(26 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Endometrial cancer (EC) is one of the most common malignancies of the female reproductive system ( 1 , 2 ). Globally, more than 200,000 women suffer from EC every year, and the mortality rate is just behind ovarian cancer and cervical cancer ( 3 ).…”

Section: Introductionmentioning

confidence: 99%

Propofol inhibits proliferation, migration, and invasion but promotes apoptosis by regulation of Sox4 in endometrial cancer cells

Liu

Zhang

et al. 2018

Braz J Med Biol Res

View full text Add to dashboard Cite

Propofol is an intravenous sedative hypnotic agent of which the growth-inhibitory effect has been reported on various cancers. However, the roles of propofol in endometrial cancer (EC) remain unclear. This study aimed to explore the effects of propofol on EC in vitro and in vivo. Different concentrations of propofol were used to treat Ishikawa cells. Colony number, cell viability, cell cycle, apoptosis, migration, and invasion were analyzed by colony formation, MTT, flow cytometry, and Transwell assays. In addition, the pcDNA3.1-Sox4 and Sox4 siRNA plasmids were transfected into Ishikawa cells to explore the relationship between propofol and Sox4 in EC cell proliferation. Tumor weight in vivo was measured by xenograft tumor model assay. Protein levels of cell cycle-related factors, apoptosis-related factors, matrix metalloproteinases 9 (MMP9), matrix metalloproteinases 2 (MMP2) and Wnt/β-catenin pathway were examined by western blot. Results showed that propofol significantly decreased colony numbers, inhibited cell viability, migration, and invasion but promoted apoptosis in a dose-dependent manner in Ishikawa cells. Moreover, propofol reduced the expression of Sox4 in a dose-dependent manner. Additionally, propofol significantly suppressed the proportions of Ki67+ cells, but Sox4 overexpression reversed the results. Furthermore, in vivo assay results showed that propofol inhibited tumor growth; however, the inhibitory effect was abolished by Sox4 overexpression. Moreover, propofol inhibited Sox4 expression via inactivation of Wnt/β-catenin signal pathway. Our study demonstrated that propofol inhibited cell proliferation, migration, and invasion but promoted apoptosis by regulation of Sox4 in EC cells. These findings might indicate a novel treatment strategy for EC.

show abstract

Section: Introductionmentioning

confidence: 99%

Propofol inhibits proliferation, migration, and invasion but promotes apoptosis by regulation of Sox4 in endometrial cancer cells

Liu

Zhang

et al. 2018

Braz J Med Biol Res

View full text Add to dashboard Cite

show abstract

“…Endometrial carcinoma (EC) is one of the most common female reproductive tract malignancies globally (1)(2)(3)(4)(5). Type I EC, additionally termed endometrioid endometrial carcinoma (EEC) or endometrioid adenocarcinoma (EAC), accounts for 80-90% of all subtypes of EC (6).…”

Section: Introductionmentioning

confidence: 99%

Bioinformatics analysis of key differentially expressed genes in well and poorly differentiated endometrial carcinoma

et al. 2018

View full text Add to dashboard Cite

Endometrial carcinoma (EC) is one of the most common gynecological malignancies. The malignant degree increases between grade (G)1 and G3, and EC of G3 usually presents a high recurrence rate and poor prognosis. Therefore, the present study aimed to examine the principal genes associated with the degree of differentiation in EC. The microarrays GSE17025, GSE24537 and GSE35784, representing data of Type I EC samples of G1 and G3, were downloaded from the Gene Expression Omnibus. The differentially expressed genes (DEGs) and differentially expressed micro (mi)RNAs (DEMs) were identified, followed by functional enrichment analyses and interaction network construction. In total, 83 upregulated and 130 downregulated DEGs with the same expression trends in two mRNA datasets were screened. The upregulated DEGs were primarily enriched in 'mitotic cell cycle process', 'cell cycle process' and 'mitotic cell cycle'; while the downregulated DEGs were enriched in 'cellular component assembly involved in morphogenesis', 'cell projection organization' and 'microtubule‑based movement'. From the protein‑protein interaction network, DNA topoisomerase IIα, kinesin family member 11, cyclin B1 and BUB1 mitotic checkpoint serine/threonine were identified as foremost hub genes. One module was extracted and involved in 'mitotic cell cycle process' and 'cell cycle process'. Based on the analysis of DEMs and the miRNA‑target regulatory network, miRNA‑9 may be the most important upregulated DEM, and the DEGs forkhead box P1 and cyclin E1 may serve vital roles in the differentiation of EC. In conclusion, principal genes were identified that may be determinants of the carcinogenesis of poorly differentiated EC, which may facilitate the examination of potential molecular mechanisms. These genes may additionally help identify candidate biomarkers and novel therapeutic targets for poorly differentiated EC.

show abstract

“…Ang II can be detected easily in atherosclerotic plaques due to its high level of expression [Hoshida et al, 2001], which can impair the function and accelerate the senescence of EPCs [Zhou et al, 2010]. This is distinct from the growth-promoting effect of Ang II in many types of cancer cells [Dominska et al, 2016;Nowakowska et al, 2016]. Although the diminished effects of Ang II on the migration, adhesion, and tube formation of EPCs can be restored by natural extracts [Parzonko et al, 2013], they are not easily administered.…”

mentioning

confidence: 99%

DJ‐1 Alleviates Angiotensin II‐Induced Endothelial Progenitor Cell Damage by Activating the PPARγ/HO‐1 Pathway

Han

Liu

Yang

2017

J of Cellular Biochemistry

View full text Add to dashboard Cite

There is evidence that angiotensin II (Ang II) may impair the functions of endothelial progenitor cells (EPCs). It was revealed that DJ-1 could resist oxidative stress. In this study, we investigated whether DJ-1 could protect EPCs against Ang II-induced cell damage. The proliferation and migration of EPCs were strongly reduced in the Ang II group and were increased by overexpression of DJ-1. Western blotting indicated that the increased expression of the senescence marker b-galactosidase and decreased expression of adhesion molecules (ICAM-1, VCAM-1) induced by Ang II were reversed after Ad-DJ-1 transfection. The reduced angiogenic capacity of EPCs caused by Ang II was also improved after Ad-DJ-1 transfection. Moreover, Ang II significantly increased the levels of reactive oxygen species (ROS), malondialdehyde (MDA), and inflammatory cytokines (TNF-a and IL-1b), reduced the levels of superoxide dismutase (SOD), glutathione (GSH), and these were reversed by Ad-DJ-1 transfection. Expression of peroxisome proliferator-activated receptor-g (PPARg) and heme oxygenase (HO-1) was increased by DJ-1. Therefore, HO-1 siRNA were constructed and transfected into EPCs, and the results showed that HO-1 siRNA transfection inhibited the effects of DJ-1 on EPC function. Thus, our study implies that DJ-1 may protect EPCs against Ang II-induced dysfunction by activating the PPARg/HO-1.

show abstract

Angiotensin II promotes endometrial cancer cell survival

Cited by 15 publications

References 30 publications

Propofol inhibits proliferation, migration, and invasion but promotes apoptosis by regulation of Sox4 in endometrial cancer cells

Propofol inhibits proliferation, migration, and invasion but promotes apoptosis by regulation of Sox4 in endometrial cancer cells

Bioinformatics analysis of key differentially expressed genes in well and poorly differentiated endometrial carcinoma

DJ‐1 Alleviates Angiotensin II‐Induced Endothelial Progenitor Cell Damage by Activating the PPARγ/HO‐1 Pathway

Contact Info

Product

Resources

About