ArticleToxicological sciences : an official journal of the Society of Toxicology2012
Cadmium increases HIF-1 and VEGF expression through ROS, ERK, and AKT signaling pathways and induces malignant transformation of human bronchial epithelial cells.
Article in Toxicological sciences : an official journal of the Society of Toxicology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers.
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88 citing papers in PubMed, 202 citations in OpenAlex.
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- Heavy Metal-Contaminated Soils and Gastric Cancer Risk: Molecular Insights and the Relevance of a One Health Perspective.International journal of molecular sciences · 2025Review
- Reactive Oxygen Species: A Double-Edged Sword in the Modulation of Cancer Signaling Pathway Dynamics.Cells · 2025Review
- Cd stabilizes HIF-1α under normoxic conditions via lysine-63-linked ubiquitination and induces ER stress and cell proliferation.Toxicological research · 2025Article
- Mechanisms of Heavy Metal Cadmium (Cd)-Induced Malignancy.Biological trace element research · 2025Review
- Toxicity Tolerance in the Carcinogenesis of Environmental Cadmium.International journal of molecular sciences · 2024Review
- The dynamic face of cadmium-induced Carcinogenesis: Mechanisms, emerging trends, and future directions.Current research in toxicology · 2024Review
- Novel Metal Nanomaterials to Promote Angiogenesis in Tissue Regeneration.Engineered regeneration · 2023Article
- The role of hypoxia-inducible factor 1 alpha (HIF-1α) modulation in heavy metal toxicity.Archives of toxicology · 2023Review
- Molecular interplay between NOX1 and autophagy in cadmium-induced prostate carcinogenesis.Free radical biology & medicine · 2023Article
- Estimation of health risks associated with dietary cadmium exposure.Archives of toxicology · 2023Review
- Disease-associated metabolic pathways affected by heavy metals and metalloid.Toxicology reports · 2023Review
- Review
- The Central Nervous Mechanism of Stress-Promoting Cancer Progression.International journal of molecular sciences · 2022Review
- Renal hypoxia-HIF-PHD-EPO signaling in transition metal nephrotoxicity: friend or foe?Archives of toxicology · 2022Review
- Melatonin Administration Prevents Placental and Fetal Changes Induced by Gestational Diabetes.Reproductive sciences (Thousand Oaks, Calif.) · 2022Article
- Impact of Air Pollution in Airway Diseases: Role of the Epithelial Cells (Cell Models and Biomarkers).International journal of molecular sciences · 2022Review
- Redox sensitive miR-27a/b/Nrf2 signaling in Cr(VI)-induced carcinogenesis.The Science of the total environment · 2022Article
- Bioinformatics analysis of key genes and potential mechanism in cadmium-induced breast cancer progression.Environmental science and pollution research international · 2022Article
- Fibroblasts mediate the angiogenesis of pheochromocytoma by increasing COX4I2 expression.Frontiers in oncology · 2022Article
28 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Cadmium is categorized as a human carcinogen especially involved in lung cancers. Angiogenesis is considered a fundamental requirement for tumorigenesis, but the mechanisms underlying the tumor angiogenesis induced by cadmium are poorly understood. Using in vitro and in vivo models, we investigated the angiogenic mechanisms of cadmium in human bronchial epithelial cells and tumor formation. Our results demonstrated that cadmium (CdCl(2)) activated extracellular signal-regulated kinases (ERK) and AKT signaling and elevated the expression of a key downstream proangiogenic molecule hypoxia-inducible factor-1 (HIF-1) in immortalized human lung epithelial BEAS-2B cells. Cadmium also induced reactive oxygen species (ROS) production, which could be inhibited by ROS scavengers, catalase and diphenyleneiodonium chloride. Inhibition of ROS generation also attenuated ERK, AKT, p70S6K1 activation, and HIF-1α expression. Similar results were obtained in normal human bronchial epithelial (NHBE) cells, showing that cadmium induced HIF-1 expression via ROS/ERK/AKT signaling pathway. Furthermore, cadmium induced vascular endothelial growth factor expression and transcriptional activation through ROS, ERK, and AKT pathways. Finally, cadmium transformed human bronchial epithelial cells in culture; the transformed cells induced tube formation in vitro, angiogenesis on chicken chorioallantoic membrane, and formed tumors in nude mice. Taken together, the results of this study provide explanation for the role and molecular mechanisms of cadmium in promoting angiogenesis in lung epithelial cells and malignant transformation and will be helpful for improved occupational protection, prevention, as well as chemotherapy of human lung cancers caused by heavy metal cadmium.
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