ArticleToxicology and applied pharmacology2018
Roles of ROS, Nrf2, and autophagy in cadmium-carcinogenesis and its prevention by sulforaphane.
Article in Toxicology and applied pharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 1 of them a synthesis that pooled it.
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
57 citing papers in PubMed, 1 synthesis or guideline pooled it, 164 citations in OpenAlex.
- Investigating the clinical efficacy, safety and molecular mechanism of sulforaphane in autism spectrum disorder: an integrated study combining meta-analysis, network pharmacology, and computational biology.BMC pharmacology & toxicology · 2025Pooled it
- Sulfur-Containing Amino Acid Homeostasis in the Central Nervous System: From Physiology Regulation to Metal-Induced Neurotoxicity.Metabolites · 2026Review
- The Thyroid Under Pressure: Heavy Metals, Endocrine Disruptors and Translational Insights into Carcinogenesis and Thyroid Dysfunctions.International journal of molecular sciences · 2026Review
- Autophagy-Apoptosis Crosstalk in Cancer: Mechanisms, Signaling Pathways, and Therapeutic Targeting.Cancers · 2026Review
- The Association Between Cadmium Exposure and Endometrial Cancer Risk: Evidence from a Comprehensive Updated Meta-Analysis.Journal of clinical medicine · 2026Review
- Gallic acid lessens kidney injury induced by inorganic arsenic and zinc oxide nanoparticles in rats via controlling electrolyte balance, oxidative stress, and Nrf-2 and HSP-90 expression.BMC pharmacology & toxicology · 2025Article
- Sulforaphane: a natural organosulfur having potential to modulate apoptosis and survival signalling in cancer.Discover oncology · 2025Review
- Nrf2: A key regulator in chemoradiotherapy resistance of osteosarcoma.Genes & diseases · 2025Review
- The Role of Heavy Metals in the Biology of Female Cancers.International journal of molecular sciences · 2025Review
- Sulforaphane alleviates renal fibrosis through dual regulation on mTOR-mediated autophagy pathway.International urology and nephrology · 2025Article
- Curcumin Treatment Ameliorates Hepatic Insulin Resistance Induced by Sub-chronic Oral Exposure to Cadmium LOAEL Dose via NF-κB and Nrf2 Pathways.Biological trace element research · 2025Article
- Mechanisms of Heavy Metal Cadmium (Cd)-Induced Malignancy.Biological trace element research · 2025Review
- Heavy Metal Exposure-induced Cardiovascular Diseases: Molecular Mechanisms and Therapeutic Role of Antioxidants.Current medicinal chemistry · 2025Review
- Carcinogenic Mechanisms of Hexavalent Chromium: From DNA Breaks to Chromosome Instability and Neoplastic Transformation.Current environmental health reports · 2024Review
- Molecular mechanisms of ferroptosis in cardiovascular disease.Molecular and cellular biochemistry · 2024Review
- Hazardous or Advantageous: Uncovering the Roles of Heavy Metals and Humic Substances in Shilajit (Phyto-mineral) with Emphasis on Heavy Metals Toxicity and Their Detoxification Mechanisms.Biological trace element research · 2024Review
- Is Cadmium Genotoxicity Due to the Induction of Redox Stress and Inflammation? A Systematic Review.Antioxidants (Basel, Switzerland) · 2024Review
- Vitamin D and Sulforaphane Decrease Inflammatory Oxidative Stress and Restore the Markers of Epithelial Integrity in an In Vitro Model of Age-Related Macular Degeneration.International journal of molecular sciences · 2024Article
- Cadmium toxicity and autophagy: a review.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2024Review
- Nanomedicine-based disulfiram and metal ion co-delivery strategies for cancer treatment.International journal of pharmaceutics: X · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
Environmental and occupational exposures to cadmium increase the risk of various cancers, including lung cancer. The carcinogenic mechanism of cadmium, including its prevention remains to be investigated. Using fluorescence and electron spin resonance spin trapping, the present study shows that in immortalized lung cells (BEAS-2BR cells), exposure cadmium generated reactive oxygen species (ROS). Through ROS generation, cadmium increased the protein level of TNF-α, which activated NF-κB and its target protein COX-2, creating an inflammatory microenvironment. As measured by anchorage-independent colony formation assay, cadmium induced malignant cell transformation. Inhibition of ROS by antioxidants inhibited transformation, showing that ROS were important in the mechanism of this process. The inflammatory microenvironment created by cadmium may also contribute to the mechanism of the transformation. Using tandem fluorescence protein mCherry-GFP-LC3 construct, the present study shows that cadmium-transformed cells had a property of autophagy deficiency, resulting in accumulation of autophagosomes and increased p62. This protein upregulated Nrf2, which also upregulated p62 through positive feed-back mechanism. Constitutive Nrf2 activation increased its downstream anti-apoptotic proteins, Bcl-2 and Bcl-xl, resulting in apoptosis resistance. In untransformed BEAS-2BR cells, sulforaphane, a natural compound, increased autophagy, activated Nrf2, and decreased ROS. In cadmium-transformed BEAS-2BR cells, sulforaphane restored autophagy, decreased Nrf2, and decreased apoptosis resistance. In untransformed cells, this sulforaphane induced inducible Nrf2 to decrease ROS and possibly malignant cell transformation. In cadmium-transformed cells, it decreased constitutive Nrf2 and reduced apoptosis resistance. The dual roles of sulforaphane make this natural compound a valuable agent for prevention against cadmium-induced carcinogenesis.
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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.