ArticleFrontiers in oncology2020
Progression-Mediated Changes in Mitochondrial Morphology Promotes Adaptation to Hypoxic Peritoneal Conditions in Serous Ovarian Cancer.
Article in Frontiers in oncology, 2020. 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, 47 citations in OpenAlex.
- Dynamic integrin expression, atypical nuclear localization, and spatial distribution during ovarian cancer progression and metastasis.Frontiers in cell and developmental biology · 2026Article
- Subcellular Stress Markers in Epithelial Ovarian Cancer.International journal of molecular sciences · 2025Review
- Unlocking the mitochondrial functional code: unraveling the pathogenesis of ovarian cancer and innovative targets to inhibit malignant behavior.Journal of translational medicine · 2025Review
- Dysregulation of Mitochondrial Function in Cancer Cells.International journal of molecular sciences · 2025Review
- Article
- Drp1 splice variants regulate ovarian cancer mitochondrial dynamics and tumor progression.EMBO reports · 2024Article
- The bioenergetic landscape of cancer.Molecular metabolism · 2024Review
- Teriflunomide/leflunomide synergize with chemotherapeutics by decreasing mitochondrial fragmentation via DRP1 in SCLC.iScience · 2024Article
- A semi-automatic method for extracting mitochondrial cristae characteristics from 3D focused ion beam scanning electron microscopy data.Communications biology · 2024Article
- Identification and characterization of stromal-like cells with CD207BMC cancer · 2024Article
- Alternative splice variants of the mitochondrial fission proteinbioRxiv : the preprint server for biology · 2024Article
- Non-Genomic Hallmarks of Aging-The Review.International journal of molecular sciences · 2023Review
- Genetic and Functional Modifications Associated with Ovarian Cancer Cell Aggregation and Limited Culture Conditions.International journal of molecular sciences · 2023Article
- Small mitochondrial protein NERCLIN regulates cardiolipin homeostasis and mitochondrial ultrastructure.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Supervised learning on impedance cytometry data for label-free biophysical distinction of pancreatic cancer cells versus their associated fibroblasts under gemcitabine treatment.Biosensors & bioelectronics · 2023Article
- Carnitine palmitoyltransferase 1A promotes mitochondrial fission by enhancing MFF succinylation in ovarian cancer.Communications biology · 2023Article
- Review
- Photochemical Targeting of Mitochondria to Overcome Chemoresistance in Ovarian CancerPhotochemistry and photobiology · 2023Review
- Ovarian Cancer: A Landscape of Mitochondria with Emphasis on Mitochondrial Dynamics.International journal of molecular sciences · 2023Review
- NLRC5 overexpression in ovarian tumors remodels the tumor microenvironment and increases T-cell reactivity toward autologous tumor-associated antigens.Frontiers in immunology · 2023Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ovarian cancer is the deadliest gynecological cancer in women, with a survival rate of less than 30% when the cancer has spread throughout the peritoneal cavity. Aggregation of cancer cells increases their viability and metastatic potential; however, there are limited studies that correlate these functional changes to specific phenotypic alterations. In this study, we investigated changes in mitochondrial morphology and dynamics during malignant transition using our MOSE cell model for progressive serous ovarian cancer. Mitochondrial morphology was changed with increasing malignancy from a filamentous network to single, enlarged organelles due to an imbalance of mitochondrial dynamic proteins (fusion: MFN1/OPA1, fission: DRP1/FIS1). These phenotypic alterations aided the adaptation to hypoxia through the promotion of autophagy and were accompanied by changes in the mitochondrial ultrastructure, mitochondrial membrane potential, and the regulation of reactive oxygen species (ROS) levels. The tumor-initiating cells increased mitochondrial fragmentation after aggregation and exposure to hypoxia that correlated well with our previously observed reduced growth and respiration in spheroids, suggesting that these alterations promote viability in non-permissive conditions. Our identification of such mitochondrial phenotypic changes in malignancy provides a model in which to identify targets for interventions aimed at suppressing metastases.
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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.