ArticleThe Journal of investigative dermatology2014
Caspase 3 promotes surviving melanoma tumor cell growth after cytotoxic therapy.
Article in The Journal of investigative dermatology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
73 citing papers in PubMed, 111 citations in OpenAlex.
- The paradigm-shifting roles of caspase-3 in cancer: from death towards resuscitation.Cancer cell international · 2026Review
- Pharmacological evaluation of 1-acetyl-β-carboline, a naturally occurring compound with anti-skin cancer potential.Molecular therapy. Oncology · 2025Article
- Nucleic acid nanobiosystems for cancer theranostics: an overview of emerging trends and challenges.Nanomedicine (London, England) · 2025Review
- Of Tingible Bodies and Starry Skies: Control of Normal and Malignant Tissues Through Apoptotic Cell-Dependent Communication (ACDC).Advances in experimental medicine and biology · 2025Review
- The Role of Caspases in Melanoma Pathogenesis.Current issues in molecular biology · 2024Review
- Discovery of Potent IsoquinolinequinoneJournal of medicinal chemistry · 2024Article
- The role of host response to chemotherapy: resistance, metastasis and clinical implications.Clinical & experimental metastasis · 2024Review
- Redox Biomarkers and Matrix Remodeling Molecules in Ovarian Cancer.Antioxidants (Basel, Switzerland) · 2024Article
- Dual‑directional effect of vinorelbine combined with cisplatin or fluorouracil on tumor growth and metastasis in metronomic chemotherapy in breast cancer.International journal of oncology · 2024Article
- Review
- Hijacking homeostasis: Regulation of the tumor microenvironment by apoptosis.Immunological reviews · 2023Review
- Extracellular vesicles arising from apoptosis: forms, functions, and applications.The Journal of pathology · 2023Review
- Chemotherapy-induced executioner caspase activation increases breast cancer malignancy through epigenetic de-repression of CDH12.Oncogenesis · 2023Article
- Messenger functions of cell death during development and homeostasis.Biochemical Society transactions · 2023Article
- Inhomogeneous mechanotransduction defines the spatial pattern of apoptosis-induced compensatory proliferation.Developmental cell · 2023Article
- Biophysics at the edge of life and death: radical control of apoptotic mechanisms.Frontiers in cell death · 2023Article
- Non-canonical roles of apoptotic and DNA double-strand break repair factors in mediating cellular response to ionizing radiation.International journal of radiation biology · 2023Review
- Characteristics and Resistance to Cisplatin of Human Neuroblastoma Cells Co-Cultivated with Immune and Stromal Cells.Bioengineering (Basel, Switzerland) · 2022Article
- Ornidazole suppresses CD133+ melanoma stem cells via inhibiting hedgehog signaling pathway and inducing multiple death pathways in a mouse model.Croatian medical journal · 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
13 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Metastatic melanoma often relapses despite cytotoxic treatment, and hence the understanding of melanoma tumor repopulation is crucial for improving our current therapies. In this study, we aim to define the role of caspase 3 in melanoma tumor growth after cytotoxic therapy. We examined a paradigm-changing hypothesis that dying melanoma cells undergoing apoptosis during cytotoxic treatment activate paracrine signaling events that promote the growth of surviving tumor cells. We propose that caspase 3 has a key role in the initiation of the release of signals from dying cells to stimulate melanoma tumor growth. We created a model for tumor cell repopulation in which a small number of luciferase-labeled, untreated melanoma cells are seeded onto a layer of a larger number of unlabeled, lethally treated melanoma cells. We found that dying melanoma cells significantly stimulate the growth of living melanoma cells in vitro and in vivo. Furthermore, we observed that caspase 3 gene knockdown attenuated the growth-stimulating effect of irradiated, dying cells on living melanoma cell growth. Finally, we showed that caspase 3-mediated dying melanoma cell stimulation of living cell growth involves secreted prostaglandin E2 (PGE2). Our study therefore suggests a counterintuitive strategy to inhibit caspase 3 for therapeutic gain in melanoma treatment.
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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.