Senescence controls prostatic neoplasia driven by Pten loss.
Maxime ParisottoElise GreletRana El BizriDaniel MetzgerPublished in: Molecular & cellular oncology (2018)
We report that Pten (phosphatase and tensin homologue) ablation in prostatic epithelial cells of adult mice promotes cell proliferation to generate prostatic intraepithelial neoplasia. Moreover, our results demonstrate that proliferating Pten-deficient cells undergo replication stress and exhibit a DNA damage response, leading to cell senescence, as seen in oncogene-induced senescence.
Keyphrases
- cell proliferation
- pi k akt
- high grade
- dna damage response
- benign prostatic hyperplasia
- cell cycle arrest
- stress induced
- endothelial cells
- dna damage
- radical prostatectomy
- high glucose
- induced apoptosis
- signaling pathway
- cell cycle
- dna repair
- prostate cancer
- single cell
- diabetic rats
- oxidative stress
- cell therapy
- type diabetes
- endoplasmic reticulum stress
- radiofrequency ablation
- drug induced
- metabolic syndrome
- wild type
- cell death
- stem cells
- heat stress
- high fat diet induced
- mesenchymal stem cells
- protein kinase
- insulin resistance
- young adults