ArticlePloS one2015
Oxidative Stress Resistance in Metastatic Prostate Cancer: Renewal by Self-Eating.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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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.
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Who cites it
19 citing papers in PubMed, 29 citations in OpenAlex.
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- Programmed Cell Death in Cancer.MedComm · 2025Review
- Mitochondrial involvement in PC: improving therapeutic strategies.Frontiers in pharmacology · 2025Review
- Cancer stem cells: advances in knowledge and implications for cancer therapy.Signal transduction and targeted therapy · 2024Review
- Article
- Unraveling the Peculiar Features of Mitochondrial Metabolism and Dynamics in Prostate Cancer.Cancers · 2023Review
- Cell-in-cell: a potential biomarker of prognosis and a novel mechanism of drug resistance in cancer.Frontiers in oncology · 2023Review
- Anoikis in phenotypic reprogramming of the prostate tumor microenvironment.Frontiers in endocrinology · 2023Review
- Addressing cancer invasion and cell motility with quantitative light microscopy.Scientific reports · 2022Article
- Impact of Androgen Deprivation on Oxidative Stress and Antioxidant Status in Nigerian Patients With Prostate Cancer Undergoing Androgen Deprivation Therapy.JCO global oncology · 2020Article
- Entosis: From Cell Biology to Clinical Cancer Pathology.Cancers · 2020Review
- Roles of cell fusion, hybridization and polyploid cell formation in cancer metastasis.World journal of clinical oncology · 2020Review
- Biological relevance of cell-in-cell in cancers.Biochemical Society transactions · 2019Review
- Cell-in-cell phenomena in cancer.Nature reviews. Cancer · 2018Review
- Quantitative phase imaging unravels new insight into dynamics of mesenchymal and amoeboid cancer cell invasion.Scientific reports · 2018Article
- Marine bisindole alkaloid: A potential apoptotic inducer in human cancer cells.European journal of histochemistry : EJH · 2018Article
- Cancer Stem Cells: Emergent Nature of Tumor Emergency.Frontiers in genetics · 2018Article
- Microenvironment-Cell Nucleus Relationship in the Context of Oxidative Stress.Frontiers in cell and developmental biology · 2018Review
- Distinctive behaviour of live biopsy-derived carcinoma cells unveiled using coherence-controlled holographic microscopy.PloS one · 2017Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Resistant cancer phenotype is a key obstacle in the successful therapy of prostate cancer. The primary aim of our study was to explore resistance mechanisms in the advanced type of prostate cancer cells (PC-3) and to clarify the role of autophagy in these processes. We performed time-lapse experiment (48 hours) with ROS generating plumbagin by using multimodal holographic microscope. Furthermore, we also performed the flow-cytometric analysis and the qRT-PCR gene expression analysis at 12 selected time points. TEM and confocal microscopy were used to verify the results. We found out that autophagy (namely mitophagy) is an important resistance mechanism. The major ROS producing mitochondria were coated by an autophagic membrane derived from endoplasmic reticulum and degraded. According to our results, increasing ROS resistance may be also accompanied by increased average cell size and polyploidization, which seems to be key resistance mechanism when connected with an escape from senescence. Many different types of cell-cell interactions were recorded including entosis, vesicular transfer, eating of dead or dying cells, and engulfment and cannibalism of living cells. Entosis was disclosed as a possible mechanism of polyploidization and enabled the long-term survival of cancer cells. Significantly reduced cell motility was found after the plumbagin treatment. We also found an extensive induction of pluripotency genes expression (NANOG, SOX2, and POU5F1) at the time-point of 20 hours. We suppose, that overexpression of pluripotency genes in the portion of prostate tumour cell population exposed to ROS leads to higher developmental plasticity and capability to faster respond to changes in the extracellular environment that could ultimately lead to an alteration of cell fate.
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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.