The marine toxin yessotoxin (YTX) can cause various cytotoxic effects depending on cell type and cell line. It is well known to trigger distinct mechanisms for programmed cell death which may overlap or cross-talk. The present contribution provides the first evidence that YTX can cause genotoxicity and induce mitotic catastrophe which can lead to different types of cell death. This work also demonstrates potential information gain from non-intrusive computer-based tracking of many individual cells during long time. Treatment of BC3H1 cells at their exponential growth phase causes atypical nuclear alterations and formation of giant cells with multiple nuclei. These are the most prominent morphological features of mitotic catastrophe. Giant cells undergo slow cell death in a necrosis-like manner. However, apoptotic-like cell death is also observed in these cells. Electron microscopy of treated BC3H1 cells reveal uncondensed chromatin and cells with double nuclei. Activation of p-p53, p-H2AX, p-Chk1, p-ATM, and p-ATR and down-regulation of p-Chk2 indicate DNA damage response and cell cycle deregulation. Micronuclei formation further support this evidence. Data from tracking single cells reveal that YTX treatment suppresses a second round of cell division in BC3H1 cells. These findings suggest that YTX can induce genomic alterations or imperfections in chromosomal segregation leading to permanent mitotic failure. This understanding extends the list of effects from YTX and which are of interest to control cancer and tumor progression.
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http://dx.doi.org/10.3389/fcell.2017.00030 | DOI Listing |
Anticancer Agents Med Chem
January 2021
Centro de Investigacao em Saude Ambiental (CISA), Escola Superior de Saude do Porto, Politecnico do Porto, Porto, Portugal.
Background: Quinoxaline-1,4-dioxide (QNX) derivatives are synthetic heterocyclic compounds with multiple biological and pharmacological effects.
Objective: In this study, we investigated the oxidative status of quinoxaline-1,4-dioxides derivatives in modulating melanoma and glioma cell lines, based on previous results from the research group and their capability to promote cell damage by the production of Reactive Oxygen Species (ROS).
Methods: Using in vitro cell cultures, the influence of 2-amino-3-cyanoquinoxaline-1,4-dioxide (2A3CQNX), 3- methyl-2-quinoxalinecarboxamide-1,4-dioxide (3M2QNXC) and 2-hydroxyphenazine-1,4-dioxide (2HF) was evaluated in metabolic activity, catalase activity, glutathione and 3-nitrotyrosine (3-NT) quantitation by HPLC in malignant melanocytes (B16-F10, MeWo) and brain tumor cells (GL-261 and BC3H1) submitted to radiotherapy treatments (total dose of 6 Gy).
Future Med Chem
April 2019
Centro de Investigação em Saúde Ambiental (CISA), Escola Superior de Saúde do Porto, Politécnico do Porto, Porto, Portugal.
Quinoxaline-1,4-dioxide derivatives are synthetic heterocyclic compounds with multiple biological and pharmacological effects. In this study, we investigated the bioactivity of five quinoxaline-1,4-di--oxides derivatives in different animal cell lines. Using cell cultures, we evaluated the influence of quinoxaline-1,4-dioxide, 2-methylquinoxaline-1,4-dioxide, 2-amino-3-cyanoquinoxaline-1,4-dioxide, 3-methyl-2-quinoxalinecarboxamide-1,4-dioxide and 2-hydroxyphenazine--dioxide (2HF) in the viability, migration and proliferation of nonmalignant (3T3-L1 and human dermal microvascular endothelial cell) and malignant (B16-F10, MeWo, GL-261 and BC3H1) cell lines.
View Article and Find Full Text PDFMol Med Rep
November 2017
Department of Neurosurgery, Tianjin Nankai Hospital, Tianjin 300100, P.R. China.
Glioblastoma is the most aggressive primary brain tumor that originates from the glial cells in adults. Aberrant angiogenesis is essential for malignant glioblastoma tumorigenesis, development and metastasis. Lenvatinib is a multi‑targeted anticancer agent that targets of receptor tyrosine kinases including vascular endothelial growth factor receptor 1 and 2, fibroblast growth factor receptor 1, platelet‑derived growth factor receptor β and v‑kit Hardy‑Zuckerman 4 feline sarcoma viral oncogene homolog.
View Article and Find Full Text PDFFront Cell Dev Biol
March 2017
Nofima ASÅs, Norway.
The marine toxin yessotoxin (YTX) can cause various cytotoxic effects depending on cell type and cell line. It is well known to trigger distinct mechanisms for programmed cell death which may overlap or cross-talk. The present contribution provides the first evidence that YTX can cause genotoxicity and induce mitotic catastrophe which can lead to different types of cell death.
View Article and Find Full Text PDFToxicol In Vitro
April 2016
Imaging Centre, Norwegian University of Life Sciences (NMBU) - Campus Ås, P.O. Box 5003, NO-1432 Ås, Norway.
The marine toxin yessotoxin (YTX) can induce programmed cell death through both caspase-dependent and -independent pathways in various cellular systems. It appears to stimulate different forms of cellular stress causing instability among cell death mechanisms and making them overlap and cross-talk. Autophagy is one of the key pathways that can be stimulated by multiple forms of cellular stress which may determine cell survival or death.
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