ReviewCancers2016
Mitochondrial Redox Signaling and Tumor Progression.
Review in Cancers, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
33 citing papers in PubMed, 77 citations in OpenAlex.
- Review
- The mitochondria as an emerging target of self-renewal in T-cell acute lymphoblastic leukemia.Cancer biology & therapy · 2025Review
- Mitochondrial Quality Control in Neurodegeneration and Cancer: A Common Denominator, Distinct Therapeutic Challenges.International journal of molecular sciences · 2025Review
- Unraveling the Complexities of Myeloid-Derived Suppressor Cells in Inflammatory Bowel Disease.International journal of molecular sciences · 2025Review
- Musculoskeletal miRNA profiling after exposure to simulated space stressors in mice.microPublication biology · 2025Article
- Analytical Methods for Assessing Thiol Antioxidants in Biological Fluids: A Review.Molecules (Basel, Switzerland) · 2024Review
- Dietary curcumin alleviates intestinal damage induced by ochratoxin A in juvenile grass carp (Animal nutrition (Zhongguo xu mu shou yi xue hui) · 2024Article
- Recent advances in mitochondria-targeting theranostic agents.Exploration (Beijing, China) · 2024Review
- Mitoferrin-1 Promotes Proliferation and Abrogates Protein Oxidation via the Glutathione Pathway in Glioblastoma.Antioxidants (Basel, Switzerland) · 2023Article
- The Impact of Oxidative Stress and AKT Pathway on Cancer Cell Functions and Its Application to Natural Products.Antioxidants (Basel, Switzerland) · 2022Review
- Article
- Mitochondrial Management of Reactive Oxygen Species.Antioxidants (Basel, Switzerland) · 2021Review
- Multifunctional Mitochondria-Targeting Nanosystems for Enhanced Anticancer Efficacy.Frontiers in bioengineering and biotechnology · 2021Review
- On the Origin of ATP Synthesis in Cancer.iScience · 2020Review
- Association between the Genetic Variants of Glutathione Peroxidase 4 and Severity of Endometriosis.International journal of environmental research and public health · 2020Article
- Mitochondrial Haplotype of the Host Stromal Microenvironment Alters Metastasis in a Non-cell Autonomous Manner.Cancer research · 2020Article
- Mitochondrial Redox Hubs as Promising Targets for Anticancer Therapy.Frontiers in oncology · 2020Review
- Biological Properties and Absolute Configuration of Flavanones FromFrontiers in pharmacology · 2020Article
- Blockade of Lactate Dehydrogenase-A (LDH-A) Improves Efficacy of Anti-Programmed Cell Death-1 (PD-1) Therapy in Melanoma.Cancers · 2019Article
- (I-3,II-3)-Biacacetin-mediated cell death involves mitochondria.Molecular and cellular biochemistry · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Cancer cell can reprogram their energy production by switching mitochondrial oxidative phosphorylation to glycolysis. However, mitochondria play multiple roles in cancer cells, including redox regulation, reactive oxygen species (ROS) generation, and apoptotic signaling. Moreover, these mitochondrial roles are integrated via multiple interconnected metabolic and redox sensitive pathways. Interestingly, mitochondrial redox proteins biphasically regulate tumor progression depending on cellular ROS levels. Low level of ROS functions as signaling messengers promoting cancer cell proliferation and cancer invasion. However, anti-cancer drug-initiated stress signaling could induce excessive ROS, which is detrimental to cancer cells. Mitochondrial redox proteins could scavenger basal ROS and function as "tumor suppressors" or prevent excessive ROS to act as "tumor promoter". Paradoxically, excessive ROS often also induce DNA mutations and/or promotes tumor metastasis at various stages of cancer progression. Targeting redox-sensitive pathways and transcriptional factors in the appropriate context offers great promise for cancer prevention and therapy. However, the therapeutics should be cancer-type and stage-dependent.
Indexed as
Identifiers
What OpenQuestion holds
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.