ArticleMolecular medicine reports2018
Propranolol suppresses the proliferation and induces the apoptosis of liver cancer cells.
Article in Molecular medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.
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Who cites it
43 citing papers in PubMed, 1 synthesis or guideline pooled it, 73 citations in OpenAlex.
- Non-selective beta-blockers and the incidence of hepatocellular carcinoma in patients with cirrhosis: a meta-analysis.Frontiers in pharmacology · 2023Pooled it
- Phase II study of propranolol feasibility with neoadjuvant chemotherapy in patients with newly diagnosed breast cancer.Breast cancer research and treatment · 2021Trial
- Neuro-immune interactions in gastrointestinal oncology: Mechanisms, challenges, and therapeutic potential.Innovation (Cambridge (Mass.)) · 2026Review
- Cancer Neoaxonogenesis: Mechanisms and Factors Involved in the Recruitment of Peripheral Nerves by Cancer Tissue.International journal of molecular sciences · 2026Review
- From single DNA molecule to nanoparticle formation: mechanistic basis for monocationic aromatic drug-induced DNA frameworks.Journal of nanobiotechnology · 2026Article
- In-silico target prediction and pathway analysis of propranolol as a potential therapeutic agent for hepatocellular carcinoma.PloS one · 2026Article
- Article
- The multifaceted impact of stress on immune function.Molecular biology reports · 2025Review
- The Road to Precision Nanomedicine: An Insight on Drug Repurposing and Advances in Nanoformulations for Treatment of Cancer.AAPS PharmSciTech · 2025Review
- Investigating the Potential of Propranolol as an Anti-Tumor Agent in Colorectal Cancer Cell Lines.International journal of molecular sciences · 2025Article
- Stress regulatory hormones and cancer: the contribution of epinephrine and cancer therapeutic value of beta blockers.Endocrine · 2025Review
- Article
- The Role of Anesthetic Management in Lung Cancer Recurrence and Metastasis: A Comprehensive Review.Journal of clinical medicine · 2024Review
- Dichloroacetate for Cancer Treatment: Some Facts and Many Doubts.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Current and Future Treatment Options for Cerebral Cavernous Malformations.Stroke (Hoboken, N.J.) · 2024Review
- Beta-blocker adjunct therapy as a prospective anti-metastatic with cardio-oncologic regulation.Clinical & experimental metastasis · 2024Review
- Potential effect of chloroquine and propranolol combination to treat colorectal and triple-negative breast cancers.Scientific reports · 2023Article
- Targeting the βThe Journal of pathology · 2023Article
- Trial watch: beta-blockers in cancer therapy.Oncoimmunology · 2023Article
- Outcomes of beta blocker use in advanced hepatocellular carcinoma treated with immune checkpoint inhibitors.Frontiers in oncology · 2023Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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.
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