ArticleMolecular and cellular biochemistry2012
Combination treatment with dihydrotanshinone I and irradiation enhances apoptotic effects in human cervical cancer by HPV E6 down-regulation and caspases activation.
Article in Molecular and cellular biochemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 29 citations in OpenAlex.
- Tackling the HuRdle of radioresistance: a radiation perspective on the RNA-binding protein HuR.Translational cancer research · 2023Article
- Targeting the RNA-Binding Protein HuR in Cancer.Cancer research · 2023Review
- Induction of ferroptosis and apoptosis in endometrial cancer cells by dihydroisotanshinone I.Heliyon · 2023Article
- Review
- Dihydrotanshinone I Inhibits the Proliferation and Growth of Oxaliplatin-Resistant Human HCT116 Colorectal Cancer Cells.Molecules (Basel, Switzerland) · 2022Article
- Enhanced Bioavailability of Dihydrotanshinone I-Bovine Serum Albumin Nanoparticles for Stroke Therapy.Frontiers in pharmacology · 2021Article
- Regulation of HuR structure and function by dihydrotanshinone-I.Nucleic acids research · 2017Article
- The herbal compound cryptotanshinone restores sensitivity in cancer cells that are resistant to the tumor necrosis factor-related apoptosis-inducing ligand.The Journal of biological chemistry · 2013Article
- Nip the HPV encoded evil in the cancer bud: HPV reshapes TRAILs and signaling landscapes.Cancer cell international · 2013Article
- Tanshinones: sources, pharmacokinetics and anti-cancer activities.International journal of molecular sciences · 2012Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aim of this study was to investigate the effect of dihydrotanshinone I (DI) in inhibiting the growth of human cervical cancer cells both in vitro and in vivo, and molecular targets in HeLa cells when treated by DI or irradiation with or without being combined. In this study, MTT, clonogenic assay, flow cytometry, and Western blotting were performed to assess the effect of treatment on cells. After treatment with IR, DI, and DI + IR, the apoptosis was 5.8, 13.3 and 22.5% (P < 0.05 vs. control), respectively. Clonogenic assay revealed that the survival of irradiated HeLa cell was significantly reduced by DI treatment. Combination treatment with IR and DI could down-regulate HPV E6 gene expression. Effect of DI on up-regulation of p21 expression and down-regulation of cyclin B1, p34(cdc2) expression in irradiated HeLa cell was concomitant with cell cycle arrest in G(2) phase. The significant increase in caspase-3 activity was also observed in the combination treatment. When HeLa cells were grown as xenografts in nude mice, combination treatment with DI and IR induced a significant decrease in tumor growth, and without signs of general or organ toxicity. These data suggest DI should be tested as the radiosensitizer in vitro and in vivo, which has potential in the treatment of human cervical cancer.
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