ArticleEnvironmental health perspectives2012
Akt activation is responsible for enhanced migratory and invasive behavior of arsenic-transformed human bronchial epithelial cells.
Article in Environmental health perspectives, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 69 citations in OpenAlex.
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- Epigenetic downregulation of OEnvironmental pollution (Barking, Essex : 1987) · 2024Article
- Loss of MEG3 contributes to the enhanced migration and invasion in arsenic-induced carcinogenesis through NQO1/FSCN1 pathway.American journal of cancer research · 2023Article
- Arsenic and cancer: Evidence and mechanisms.Advances in pharmacology (San Diego, Calif.) · 2023Article
- Chronic Hexavalent Chromium Exposure Upregulates the RNA Methyltransferase METTL3 Expression to Promote Cell Transformation, Cancer Stem Cell-Like Property, and Tumorigenesis.Toxicological sciences : an official journal of the Society of Toxicology · 2022Article
- Arsenic and Human Health: Genotoxicity, Epigenomic Effects, and Cancer Signaling.Biological trace element research · 2022Review
- Chronic and acute arsenic exposure enhance EGFR expression via distinct molecular mechanisms.Toxicology in vitro : an international journal published in association with BIBRA · 2020Article
- Arsenic and benzo[a]pyrene co-exposure acts synergistically in inducing cancer stem cell-like property and tumorigenesis by epigenetically down-regulating SOCS3 expression.Environment international · 2020Article
- Metal carcinogen exposure induces cancer stem cell-like property through epigenetic reprograming: A novel mechanism of metal carcinogenesis.Seminars in cancer biology · 2019Review
- Synthesis and biological evaluation of quercetin-zinc (II) complex for anti-cancer and anti-metastasis of human bladder cancer cells.In vitro cellular & developmental biology. Animal · 2019Article
- A review of arsenic exposure and lung cancer.Toxicology research · 2019Review
- Chronic low dose arsenic exposure preferentially perturbs mitotic phase of the cell cycle.Genes & cancer · 2019Article
- PI3K/Akt/mTOR Signaling Pathway and the Biphasic Effect of Arsenic in Carcinogenesis.Molecular pharmacology · 2018Review
- Laminar shear stress inhibits high glucose-induced migration and invasion in human bladder cancer cells.In vitro cellular & developmental biology. Animal · 2018Article
- Article
- Gestational Exposure to Sidestream (Secondhand) Cigarette Smoke Promotes Transgenerational Epigenetic Transmission of Exacerbated Allergic Asthma and Bronchopulmonary Dysplasia.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- Persistent Exposure toFrontiers in cellular and infection microbiology · 2017Article
- The role of microRNAs in metal carcinogen-induced cell malignant transformation and tumorigenesis.Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association · 2016Review
- 17β-Estradiol Inhibites Tumor Necrosis Factor-α Induced Apoptosis of Human Nucleus Pulposus Cells via the PI3K/Akt Pathway.Medical science monitor : international medical journal of experimental and clinical research · 2016Article
- Functional role of inorganic trace elements in angiogenesis part III: (Ti, Li, Ce, As, Hg, Va, Nb and Pb).Critical reviews in oncology/hematology · 2016Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundArsenic is one of the most common environmental contaminants. Long-term exposure to arsenic causes human bronchial epithelial cell (HBEC) malignant transformation and lung cancer. However, the mechanism of arsenic lung carcinogenesis is not clear, and the migratory and invasive properties of arsenic-transformed cells (As-transformed cells) have rarely been studied.
objectivesThis study was designed to investigate the migratory and invasive behavior of As-transformed HBECs and the underlying mechanism.
methodsAs-transformed p53lowHBECs were generated by exposing p53-knockdown HBECs to sodium arsenite (2.5 μM) for 16 weeks. Cell migration was assessed by transwell migration and wound-healing assay. Cell invasion was evaluated using Matrigel-coated transwell chambers. Gene overexpression, small interfering RNA (siRNA) knockdowns, and pharmacological inhibitors were used to determine the potential mechanism responsible for enhanced cell migration and invasion.
resultsTranswell migration and invasion assays revealed that As-transformed p53lowHBECs were highly migratory and invasive. Akt (also known as protein kinase B) and extracellular signal-regulated protein kinase 1/2 (Erk1/2) were strongly activated in As-transformed p53lowHBECs. Stable expression of microRNA 200b in As-transformed p53lowHBECs abolished Akt and Erk1/2 activation and completely suppressed cell migration and invasion. Pharmacological inactivation of Akt but not Erk1/2 significantly decreased cell migration and invasion. Inhibition of Akt reduced the expression of epithelial-to-mesenchymal transition-inducing transcription factors zinc-finger E-box-binding homeobox factor 1 (ZEB1) and ZEB2. siRNA knockdown of ZEB1 and ZEB2 impaired As-transformed p53lowHBEC migration and invasion.
conclusionsAkt activation plays a critical role in enabling As-transformed HBEC migration and invasion by promoting ZEB1 and ZEB2 expression.
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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.