Silencing of angiotensin receptor 1 interferes with angiotensin II oncogenic activity in endometrial cancer.
Zuzanna E Matysiak-BurzyńskaMagdalena NowakowskaKamila DomińskaKarolina KowalskaElżbieta PłuciennikAgnieszka Wanda Piastowska CiesielskaPublished in: Journal of cellular biochemistry (2018)
In mammalian cells, angiotensin II (AngII) binds to 2 distinct high-affinity plasma membrane receptors: angiotensin receptor 1 (AT1R) and angiotensin receptor 2 (AT2R). Healthy human endometrium from women of reproductive age expresses all of the components of the renin-angiotensin system. Many studies suggest that AngII, acting via AT1R, may have a role in the development and progression of cancer, which changes the expression of angiogenic factors, AngII and AT1R are correlated with the presence of endometrial cancer (EC). The aim of the current study was to identify the effects of AngII on the proliferation, cell cycle progression, apoptosis and mobility of ISHIKAWA, MFE296 and MFE280 EC cells with silenced AT1R. It also examines epithelial-mesenchymal transition markers by gene expression analysis. The obtained results suggest that the silencing of AT1R expression alters the migration and invasion ability of EC cells. However, this silencing is not sufficient to inhibit the effects of AngII on EC cells, suggesting that AngII plays a more complex role in the development of EC.
Keyphrases
- angiotensin ii
- endometrial cancer
- angiotensin converting enzyme
- cell cycle arrest
- induced apoptosis
- cell cycle
- vascular smooth muscle cells
- endoplasmic reticulum stress
- epithelial mesenchymal transition
- cell death
- signaling pathway
- poor prognosis
- pi k akt
- cell proliferation
- oxidative stress
- endothelial cells
- squamous cell carcinoma
- genome wide
- metabolic syndrome
- long non coding rna
- skeletal muscle
- papillary thyroid
- copy number
- transforming growth factor