ArticleMolecular pharmaceutics2019
p53-Bad: A Novel Tumor Suppressor/Proapoptotic Factor Hybrid Directed to the Mitochondria for Ovarian Cancer Gene Therapy.
Article in Molecular pharmaceutics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 19 citations in OpenAlex.
- Natural products targeting cytokine-regulated SASP inflammation networks in Ovarian cancer: Implications on immune escape and molecular resistance.Inflammopharmacology · 2026Review
- Catechin-Folate nano-niosomes from Osbeckia parvifolia Arn. induce apoptotic cell death in Ovarian cancer.Scientific reports · 2026Article
- Mitochondrially Targeted p53-Bad* Fusion Gene Therapy Promotes Apoptosis in Hepatocellular Carcinoma by Pan-Bcl-2 Inhibition.Molecular pharmaceutics · 2025Article
- Unlocking the mitochondrial functional code: unraveling the pathogenesis of ovarian cancer and innovative targets to inhibit malignant behavior.Journal of translational medicine · 2025Review
- Oncogenic Pathways and Targeted Therapies in Ovarian Cancer.Biomolecules · 2024Review
- Review
- Suicide gene strategies applied in ovarian cancer studies.Cancer gene therapy · 2023Review
- The Challenges and Prospects of p53-Based Therapies in Ovarian Cancer.Biomolecules · 2023Review
- p53-Bad* Fusion Gene Therapy Induces Apoptosis In Vitro and Reduces Zebrafish Tumor Burden in Hepatocellular Carcinoma.Molecular pharmaceutics · 2023Article
- La protein regulates protein expression by binding with the mRNAs of target genes and participates the pathological process of ovarian cancer.Frontiers in oncology · 2022Article
- Emerging role of BAD and DAD1 as potential targets and biomarkers in cancer.Oncology letters · 2021Review
- CMBs carrying PTX and CRISPR/Cas9 targetingMolecular medicine reports · 2021Article
- Targeting multiple genes containing long mononucleotide A-T repeats in lung cancer stem cells.Journal of translational medicine · 2021Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Clinical trials involving p53 gene therapy for ovarian cancer failed due to the dominant negative inhibition of wild-type p53 and multiple genetic aberrations in ovarian cancer. To overcome this problem, we have designed a more potent chimeric gene fusion, called p53-Bad, that combines p53 with the mitochondrial pro-apoptotic factor Bad. Unlike wild-type p53, which acts as a nuclear transcription factor, this novel p53-Bad construct has multiple unique mechanisms of action including a direct and rapid apoptotic effect at the mitochondria. The mitochondrial localization, transcription activity, and apoptotic activity of the constructs were tested. The results suggest that p53 can be effectively targeted to the mitochondria by controlling the phosphorylation of pro-apoptotic Bad, which can only localize to the mitochondria when Ser-112 and Ser-136 of Bad are unphosphorylated. By introducing S112A and S136A mutations, p53-Bad fusion cannot be phosphorylated at these two sites and always localizes to the mitochondria. p53-Bad constructs also have superior activity over p53 and Bad alone. The apoptotic activity is consistent in many ovarian cancer cell lines regardless of the endogenous p53 status. Both p53 and the BH3 domain of Bad contribute to the superior activity of p53-Bad. Our data suggests that p53-Bad fusions are capable of inducing apoptosis and should be further pursued for gene therapy for ovarian cancer.
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