ArticleCancer science2023
Shikonin reverses pyruvate kinase isoform M2-mediated propranolol resistance in infantile hemangioma through reactive oxygen species-induced autophagic dysfunction.
Article in Cancer science, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 9 citations in OpenAlex.
- Targeting Pyruvate Kinase M2: Signal Transduction Pathways and Exploration of Cancer Therapeutic Strategies.The AAPS journal · 2026Review
- Analysis of Necroptosis-Related Genes and Immune Cell Infiltration in Infantile Hemangioma.Endocrine, metabolic & immune disorders drug targets · 2026Article
- Transdermal delivery of timolol maleate using hydrogel microneedles for the treatment of infantile haemangiomas.Materials today. Bio · 2025Article
- Tumor microenvironment: recent advances in understanding and its role in modulating cancer therapies.Medical oncology (Northwood, London, England) · 2025Review
- Decoding infantile hemangioma: cellular dynamics, molecular signals, and microenvironmental influences.Frontiers in oncology · 2025Review
- Infantile hemangioma models: is the needle in a haystack?Journal of translational medicine · 2023Review
- Shikonin reverses pyruvate kinase isoform M2-mediated propranolol resistance in infantile hemangioma through reactive oxygen species-induced autophagic dysfunction.Cancer science · 2023Article
- Editorial: Advances in the medical management of infantile hemangioma.Frontiers in oncology · 2023Article
- Integrated nontargeted and targeted metabolomics analyses amino acids metabolism in infantile hemangioma.Frontiers in oncology · 2023Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Infantile hemangioma (IH) is the most common benign tumor in infancy. Propranolol, a nonselective β-adrenergic receptor blocker, is now the first-line therapy for IH. Recently, low sensitivity to propranolol therapy has become one major reason for the failure of IH treatment. However, the exact underlying mechanisms are yet to be fully elucidated. Here, we reported that pyruvate kinase isoform M2 (PKM2), an essential glycolytic enzyme, played a critical role in regulating the progression of IH and the therapeutic resistance of propranolol treatment. Shikonin reversed the propranolol resistance in hemangioma-derived endothelial cells and in hemangioma animal models. Moreover, shikonin combined with propranolol could induce excessive reactive oxygen species (ROS) accumulation and lead to autophagic dysfunction, which is essential for the enhanced therapeutic sensitivity of propranolol treatment. Taken together, our results indicated that PKM2 has a significant role in hemangiomas progression and therapeutic resistance; it could be a safe and effective therapeutic strategy for those hemangiomas with poor propranolol sensitivity combined with shikonin.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.