ArticleInternational journal of molecular sciences2022
Apoptosis as Driver of Therapy-Induced Cancer Repopulation and Acquired Cell-Resistance (CRAC): A Simple In Vitro Model of Phoenix Rising in Prostate Cancer.
Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
21 citing papers in PubMed, 28 citations in OpenAlex.
- The dark side of apoptosis: how dying cells fuel tumor angiogenesis.Apoptosis : an international journal on programmed cell death · 2026Article
- The paradigm-shifting roles of caspase-3 in cancer: from death towards resuscitation.Cancer cell international · 2026Review
- Genome agnostic, multi-level non-oncogene addiction-based systems pharmacology for rescuing metastatic relapsed/refractory neoplasias.Frontiers in pharmacology · 2026Review
- Dysfunctional, Tissue-Resident, Very Small Embryonic-Like Stem Cells (VSELs) Initiate Cancer and Result in its Progression and Metastasis, Independent of Epithelial-Mesenchymal Transition.Stem cell reviews and reports · 2026Review
- What Is Apoptosis and Why Is It Inhibited by the Most Important Tumor Suppressor (p53)?International journal of molecular sciences · 2025Review
- Magnetic Hyperthermia with Iron Oxide Nanoparticles: From Toxicity Challenges to Cancer Applications.Nanomaterials (Basel, Switzerland) · 2025Review
- Anastasis and Other Apoptosis-Related Prosurvival Pathways Call for a Paradigm Shift in Oncology: Significance of Deintensification in Treating Solid Tumors.International journal of molecular sciences · 2025Review
- Changing the Landscape of Solid Tumor Therapy from Apoptosis-Promoting to Apoptosis-Inhibiting Strategies.Current issues in molecular biology · 2024Review
- Single-Cell MTT: A Simple and Sensitive Assay for Determining the Viability and Metabolic Activity of Polyploid Giant Cancer Cells (PGCCs).Methods in molecular biology (Clifton, N.J.) · 2024Article
- Review
- Intratumor Heterogeneity and Treatment Resistance of Solid Tumors with a Focus on Polyploid/Senescent Giant Cancer Cells (PGCCs).International journal of molecular sciences · 2023Review
- Safe-Shields: Basal and Anti-UV Protection of Human Keratinocytes by Redox-Active Cerium Oxide Nanoparticles Prevents UVB-Induced Mutagenesis.Antioxidants (Basel, Switzerland) · 2023Article
- Androgen Deprivation Freezes Hormone-Sensitive Prostate Cancer Cells in a Reversible, Genetically Unstable Quasi-Apoptotic State, Bursting into Full Apoptosis upon Poly(ADP-ribose) Polymerase Inhibition.International journal of molecular sciences · 2023Article
- Peroxisome proliferator-activated receptorα/γ agonist pioglitazone for rescuing relapsed or refractory neoplasias by unlocking phenotypic plasticity.Frontiers in oncology · 2023Review
- Cancer cell repopulation after therapy: which is the mechanism?Oncoscience · 2023Article
- Metabolic Reprogramming of Castration-Resistant Prostate Cancer Cells as a Response to Chemotherapy.Metabolites · 2022Article
- What Are the Reasons for Continuing Failures in Cancer Therapy? Are Misleading/Inappropriate Preclinical Assays to Be Blamed? Might Some Modern Therapies Cause More Harm than Benefit?International journal of molecular sciences · 2022Review
- Review
- Editorial: Anakoinosis for promoting tumor tissue editing: Novel therapeutic opportunities for establishing clinically relevant tumor control by targeting tumor plasticity.Frontiers in oncology · 2022Article
- Apoptosis inhibition restrains primary malignant traits in differentFrontiers in cell and developmental biology · 2022Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 3 countries.
Funding
Abstract
Apoptotic cells stimulate compensatory proliferation through the caspase-3-cPLA-2-COX-2-PGE-2-STAT3 Phoenix Rising pathway as a healing process in normal tissues. Phoenix Rising is however usurped in cancer, potentially nullifying pro-apoptotic therapies. Cytotoxic therapies also promote cancer cell plasticity through epigenetic reprogramming, leading to epithelial-to-mesenchymal-transition (EMT), chemo-resistance and tumor progression. We explored the relationship between such scenarios, setting-up an innovative, straightforward one-pot in vitro model of therapy-induced prostate cancer repopulation. Cancer (castration-resistant PC3 and androgen-sensitive LNCaP), or normal (RWPE-1) prostate cells, are treated with etoposide and left recovering for 18 days. After a robust apoptotic phase, PC3 setup a coordinate tissue-like response, repopulating and acquiring EMT and chemo-resistance; repopulation occurs via Phoenix Rising, being dependent on high PGE-2 levels achieved through caspase-3-promoted signaling; epigenetic inhibitors interrupt Phoenix Rising after PGE-2, preventing repopulation. Instead, RWPE-1 repopulate via Phoenix Rising without reprogramming, EMT or chemo-resistance, indicating that only cancer cells require reprogramming to complete Phoenix Rising. Intriguingly, LNCaP stop Phoenix-Rising after PGE-2, failing repopulating, suggesting that the propensity to engage/complete Phoenix Rising may influence the outcome of pro-apoptotic therapies. Concluding, we established a reliable system where to study prostate cancer repopulation, showing that epigenetic reprogramming assists Phoenix Rising to promote post-therapy cancer repopulation and acquired cell-resistance (CRAC).
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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.