ArticleOncotarget2015
Role of miR-182 in response to oxidative stress in the cell fate of human fallopian tube epithelial cells.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
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
20 citing papers in PubMed, 45 citations in OpenAlex.
- Norepinephrine induces anoikis resistance in high-grade serous ovarian cancer precursor cells.JCI insight · 2024Article
- The roles of miRNAs in adult skeletal muscle satellite cells.Free radical biology & medicine · 2023Review
- Article
- Identification and Validation of an Aging-Associated circRNA-miRNA-mRNA Network in Neovascular Age-Related Macular Degeneration.Gerontology · 2023Article
- Review
- Revisiting therapeutic strategies for ovarian cancer by focusing on redox homeostasis.Oncology letters · 2022Review
- MicroRNAs, Long Non-Coding RNAs, and Circular RNAs in the Redox Control of Cell Senescence.Antioxidants (Basel, Switzerland) · 2022Review
- Cellular models of development of ovarian high-grade serous carcinoma: A review of cell of origin and mechanisms of carcinogenesis.Cell proliferation · 2021Review
- miR-181a initiates and perpetuates oncogenic transformation through the regulation of innate immune signaling.Nature communications · 2020Article
- MicroRNA and ROS Crosstalk in Cardiac and Pulmonary Diseases.International journal of molecular sciences · 2020Review
- Fallopian tube initiation of high grade serous ovarian cancer and ovarian metastasis: Mechanisms and therapeutic implications.Cancer letters · 2020Review
- Role of Reactive Oxygen Species in Cancer Progression: Molecular Mechanisms and Recent Advancements.Biomolecules · 2019Review
- MicroRNA Networks Modulate Oxidative Stress in Cancer.International journal of molecular sciences · 2019Review
- Tetramethylpyrazine protects retinal ganglion cells against H2O2‑induced damage via the microRNA‑182/mitochondrial pathway.International journal of molecular medicine · 2019Article
- Oxidative stress-induced miRNAs modulate AKT signaling and promote cellular senescence in uterine leiomyoma.Journal of molecular medicine (Berlin, Germany) · 2018Article
- Arsenic trioxide-mediated suppression of miR-182-5p is associated with potent anti-oxidant effects through up-regulation ofOncotarget · 2018Article
- A step-by-step microRNA guide to cancer development and metastasis.Cellular oncology (Dordrecht, Netherlands) · 2017Review
- MicroRNA Regulation of Oxidative Stress-Induced Cellular Senescence.Oxidative medicine and cellular longevity · 2017Review
- Dysregulation and functional roles of miR-183-96-182 cluster in cancer cell proliferation, invasion and metastasis.Oncotarget · 2016Review
- Interplay between Reactive oxygen Species and MicroRNAs in Cancer.Current pharmacology reports · 2016Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
High grade serous ovarian carcinoma (HGSC) is a DNA instable tumor and its precursor is commonly found originating from the fimbriated end of the fallopian tube secretory epithelial (FTSE) cells. The local stresses via ovulation and related inflammation are risks for HGSC. In this study, we examined the cellular and molecular responses of FTSE cells to stress. We found that excess intracellular reactive oxygen species (ROS) in normal FTSE cells upregulated a subset of microRNA expression (defined as ROSmiRs). Most ROSmiRs' expression and function were influenced and regulated by p53, and together they drove the cells into stress-induced premature senescence (SIPS). However, ROS-induced miR-182 is regulated by β-catenin, not by p53. In normal FTSE cells, miR-182 overexpression triggers cellular senescence by p53-mediated upregulation of p21. Conversely, in cells with p53 mutations, miR-182 overexpression no longer enhances p21 but functions as an "Onco-miR". p53 dysfunction is a prerequisite for miR-182-mediated tumorigenesis. In addition, we found that human follicular fluid could significantly induce intracellular ROS in normal FTSE cells. These findings suggest that ROS and p53 mutations may trigger a series of events, beginning with overexpressing miR-182 by ROS and β-catenin, impairing the DNA damage response, promoting DNA instability, bypassing senescence and eventually leading to DNA instable tumors in FTSE cells.
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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.