Amaravadi, R., Kimmelman, A. C. & White, E. Recent insights into the function of autophagy in cancer. 2013 Dec;16(4):315-22. doi: 10.1038/pcan.2013.38. Propranolol comes in the form of tablets, capsules, an oral solution (Hemangeol) and a solution used for injection. There is accumulating evidence that β-2 adrenergic receptor (ADRB2) signaling contributes to the progression and therapy resistance of prostate cancer, whereas availability of clinically tested β-blocker propranolol makes this pathway especially attractive as … Scientific Reports Zhang, P., Verity, M. A.
Epub 2018 Aug 8.Chiu SC, Huang SY, Chen SP, Su CC, Chiu TL, Pang CY.Prostate Cancer Prostatic Dis. To select patients for clinical trials of propranolol three classes of biomarkers are proposed. eCollection 2019. Propranolol blocks autophagy in PC3 cells and induces a massive accumulation of autophagosomes. Zhang, P. & Reue, K. Lipin proteins and glycerolipid metabolism: Roles at the ER membrane and beyond. Propranolol was reported to block the late phase of autophagy. Sodium pyruvate, sodium cacodylate, glutamine, glucose, carbonyl cyanide 4-(trifluoromethoxy)-phenylhydrazone (FCCP), oligomycin, rotenone, antimycin A, 2-deoxy-D-glucose (D6134), (±)-propranolol hydrochloride (P0884) were from Sigma (Darmstadt, Germany). TMRE is a cationic dye that is rapidly accumulated by mitochondria. Brown, J. Human prostate adenocarcinoma cells (PC3) were grown in Ham’s F-12K medium (Invitrogen, Merelbeke, Belgium) complemented by 7% Foetal Bovine Serum (FBS) (Lonza, Verviers, Belgium) or cultured in DMEM (Lonza) supplemented with 7% dialyzed FBS and different concentrations of glucose. 2019 Aug 8;9:745. doi: 10.3389/fonc.2019.00745. 10Autophagy flux was investigated using the reporter plasmid pBABE-puro-mCherry-EGFP-LC3B (Addgene) as reported previouslyCell survival and apoptosis were evaluated by FACS analysis following manufacturer instructions of the Annexin V-FITC Apoptosis Detection kit (Sigma). 16411973200, 19411971700). Ultrathin sections (70 nm thick) were obtained by using an ultramicrotome (Reichert Ultracut E Leica, Wetzlar, Germany), equipped with a diamond knife (Diatome, Hatfield, Pennsylvania). You can also search for this author in PC3 cells were treated with 2DG (2DG) (10 mM), propranolol (P) (100 µM) or both for 24 h. PC3 cells were analyzed for mitochondrial bioenergetics using the Agilent Seahorse XF technology. We retrospectively assessed the impact of propranolol treatment on HCC occurrence in a cohort of 291 patients with compensated viral C (HCV) cirrhosis, prospectively followed and screened …
The ultrathin sections were observed under a JEM-1400 transmission electron microscope (Jeol, Croissy Sur Seine, France) at 80 kV and micrographs were taken with an 11 MegaPixel bottom-mounted TEM camera system (Quemesa, Olympus, Münster, Germany).Experimental protocol was approved by the ethical committee of the University of Liège (approval document n°1701) according to the European Communities Council Directive. Here, we report that treatment of cancer cells with propranolol in combination with the glycolysis inhibitor 2DG induced a massive accumulation of autophagosome due to autophagy blockade. First, biomarkers of ADRB2/cAMP-dependent protein kinase (PKA) pathway activation; second, biomarkers that inform about activation of other signaling pathways unrelated to ADRB2; third, apoptosis regulatory molecules controlled by ADRB2 signaling and other survival signaling pathways. PC3 cells were treated with 2DG (10 mM), propranolol (P) (100 µM), or both together, and were collected at the indicated times. Propranolol inhibits cell viability and migration of prostate cancer treated by ADT: After 72 h the cell viability assay was conducted and data was shown in Fig. Epub 2016 Sep 24.Front Oncol. Clipboard, Search History, and several other advanced features are temporarily unavailable. The author declares no conflict of interest. (Glycolysis blockade by 2DG induced an increase of autophagy flux in PC3 cells. Boyden chamber cell migration assay results were shown in Fig. The progression from CRPC to is a major negative consequence of prostate cancer therapy CREB is a transcription factor that is highly expressed in a variety of tumors. PC3 cells were cultured in medium containing 7% dialyzed FBS and 1 mM or 7 mM glucose for the indicated times. Inhibition of apoptosis is one of the major mechanisms by which activation of ADRB2 contributes to prostate cancer pathophysiology.
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