ArticleOncotarget2014
The induction of the p53 tumor suppressor protein bridges the apoptotic and autophagic signaling pathways to regulate cell death in prostate cancer cells.
Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 42 citations in OpenAlex.
- Review
- Advancements and limitations in traditional anti-cancer therapies: a comprehensive review of surgery, chemotherapy, radiation therapy, and hormonal therapy.Discover oncology · 2025Review
- From regulation to deregulation of p53 in hematologic malignancies: implications for diagnosis, prognosis and therapy.Biomarker research · 2024Review
- Review
- MDM2- an indispensable player in tumorigenesis.Molecular biology reports · 2023Review
- Expansion of human amniotic epithelial cells using condition cell reprogramming technology.Human cell · 2023Article
- A novel chemo-phenotypic method identifies mixtures of salpn, vitamin D3, and pesticides involved in the development of colorectal and pancreatic cancer.Ecotoxicology and environmental safety · 2022Article
- Regulation of Chemosensitivity in Human Medulloblastoma Cells by p53 and the PI3 Kinase Signaling Pathway.Molecular cancer research : MCR · 2022Article
- The Effect of Arbutin on The Expression of Tumor SuppressorCell journal · 2021Article
- Autophagy-related genes are potential diagnostic and prognostic biomarkers in prostate cancer.Translational andrology and urology · 2020Article
- Article
- Culture and application of conditionally reprogrammed primary tumor cells.Gastroenterology report · 2020Review
- Conditional reprogramming: Modeling urological cancer and translation to clinics.Clinical and translational medicine · 2020Review
- The Sustained Induction of c-MYC Drives Nab-Paclitaxel Resistance in Primary Pancreatic Ductal Carcinoma Cells.Molecular cancer research : MCR · 2019Article
- Human ex vivo 3D bone model recapitulates osteocyte response to metastatic prostate cancer.Scientific reports · 2018Article
- Mutations of p53 decrease sensitivity to the anthracycline treatments in bladder cancer cells.Oncotarget · 2018Article
- Pseudo-Ginsenoside Rh2 induces A549 cells apoptosis via the Ras/Raf/ERK/p53 pathway.Experimental and therapeutic medicine · 2018Article
- p53 and metabolism: from mechanism to therapeutics.Oncotarget · 2018Review
- Characterization of the effects of defined, multidimensional culture conditions on conditionally reprogrammed primary human prostate cells.Oncotarget · 2018Article
- Article
Corrections and comments
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Authors and funding
23 authors at 5 institutions in 1 country.
Funding
Abstract
The p53 tumor suppressor protein plays a crucial role in influencing cell fate decisions in response to cellular stress. As p53 elicits cell cycle arrest, senescence or apoptosis, the integrity of the p53 pathway is considered a key determinant of anti-tumor responses. p53 can also promote autophagy, however the role of p53-dependent autophagy in chemosensitivity is poorly understood. VMY-1-103 (VMY), a dansylated analog of purvalanol B, displays rapid and potent anti-tumor activities, however the pathways by which VMY works are not fully defined. Using established prostate cancer cell lines and novel conditionally reprogrammed cells (CRCs) derived from prostate cancer patients; we have defined the mechanisms of VMY-induced prostate cancer cell death. Herein, we show that the cytotoxic effects of VMY required a p53-dependent induction of autophagy, and that inhibition of autophagy abrogated VMY-induced cell death. Cancer cell lines harboring p53 missense mutations evaded VMY toxicity and treatment with a small molecule compound that restores p53 activity re-established VMY-induced cell death. The elucidation of the molecular mechanisms governing VMY-dependent cell death in cell lines, and importantly in CRCs, provides the rationale for clinical studies of VMY, alone or in combination with p53 reactivating compounds, in human prostate cancer.
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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.