Abstract:
:An increasing amount of evidence indicates that the inhibition of β adrenergic signaling can result in the inhibition of tumor growth. However, the role of propranolol in liver cancer and the underlying mechanism remain to be elucidated. The present study aimed to investigate the role of propranolol in liver cancer cell lines and provide evidence for further clinical study. Propranolol was added at different concentrations to HepG2 and HepG2.2.15 liver cancer cells and HL‑7702 normal human liver cells. The proliferation of the cell lines was monitored by live‑cell imaging at a range of time intervals. Immunofluorescence using DAPI and Hoechst 33342/propidium iodide (PI) staining, Annexin V‑FITC/PI double‑staining flow cytometry, western blotting and reverse transcription‑quantitative polymerase chain reaction were used to investigate the effect of propranolol on liver cancer cell apoptosis. The proliferation of HepG2 and HepG2.2.15 cells was inhibited by 40 and 80 µmol/l propranolol. However, the proliferation of HL‑7702 cells was not affected by <160 µmol/l propranolol. Propranolol treatment decreased the expression of adrenergic receptor β‑2 to a greater extent than adrenergic receptor β‑1, and induced apoptosis in the liver cancer cells. The apoptotic rates of HepG2 and HepG2.2.15 cells increased following treatment with propranolol, while the apoptotic rate of HL‑7702 cells was not affected. Propranolol promoted poly (ADP‑ribose) polymerase cleavage and decreased the expression of full‑length caspase‑3 in liver cancer cell lines; it induced S‑phase arrest in HepG2 and HepG2.2.15 cell lines, while HL‑7702 cells were arrested at the G0/G1 phase of the cell cycle. Thus, it was demonstrated that propranolol inhibited proliferation, promoted apoptosis and induced S-phase arrest in HepG2 and HepG2.2.15 cells.
journal_name
Mol Med Repjournal_title
Molecular medicine reportsauthors
Wang F,Liu H,Wang F,Xu R,Wang P,Tang F,Zhang X,Zhu Z,Lv H,Han Tdoi
10.3892/mmr.2018.8476subject
Has Abstractpub_date
2018-04-01 00:00:00pages
5213-5221issue
4eissn
1791-2997issn
1791-3004journal_volume
17pub_type
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