ArticleOncotarget2016
Hexavalent chromium induces malignant transformation of human lung bronchial epithelial cells via ROS-dependent activation of miR-21-PDCD4 signaling.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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
32 citing papers in PubMed, 57 citations in OpenAlex.
- Integration of epigenetics into ecotoxicology: insights and fundamental research needs.Biological reviews of the Cambridge Philosophical Society · 2026Review
- The Dual Role of Dietary Phytochemicals in Oxidative Stress: Implications for Oncogenesis, Cancer Chemoprevention, and ncRNA Regulation.Antioxidants (Basel, Switzerland) · 2025Review
- Nrf2/cyclooxygenase 2 signaling in Cr(VI)-induced carcinogenesis.Ecotoxicology and environmental safety · 2025Article
- Enrichment of RedoxifibromiR miR-21-5p in Plasma Exosomes of Hypertensive Patients with Renal Injury.International journal of molecular sciences · 2025Article
- Investigating the heavy metal (Hg, Cd, Pb, Cr, As) binding affinity and sensing capability of 2-((2-(hydroxymethyl)quinolin-8-yl)oxy)-N-(quinolin-8-yl)acetamide.Frontiers in chemistry · 2025Article
- Carcinogenic Mechanisms of Hexavalent Chromium: From DNA Breaks to Chromosome Instability and Neoplastic Transformation.Current environmental health reports · 2024Review
- The interaction between miRNAs and hazardous materials.Non-coding RNA research · 2023Review
- Long Non-Coding RNA MEG3 in Metal Carcinogenesis.Toxics · 2023Review
- Epigenetic and epitranscriptomic mechanisms of chromium carcinogenesis.Advances in pharmacology (San Diego, Calif.) · 2023Article
- MicroRNA-Gene Interactions Impacted by Toxic Metal(oid)s during EMT and Carcinogenesis.Cancers · 2022Review
- Review
- Epigenetic alterations of CXCL5 in Cr(VI)-induced carcinogenesis.The Science of the total environment · 2022Article
- Loss of MEG3 and upregulation of miR-145 play an important role in the invasion and migration of Cr(VI)-transformed cells.Heliyon · 2022Article
- Epigenetic Regulation in Exposome-Induced Tumorigenesis: Emerging Roles of ncRNAs.Biomolecules · 2022Review
- The crosstalk between reactive oxygen species and noncoding RNAs: from cancer code to drug role.Molecular cancer · 2022Review
- Epigenetic mechanisms in metal carcinogenesis.Toxicology reports · 2022Review
- Dysregulation of microRNAs in metal-induced angiogenesis and carcinogenesis.Seminars in cancer biology · 2021Review
- Assessment of Mechanistic Data for Hexavalent Chromium-Induced Rodent Intestinal Cancer Using the Key Characteristics of Carcinogens.Toxicological sciences : an official journal of the Society of Toxicology · 2021Article
- MicroRNA expression in lung tissues of asbestos-exposed mice: Upregulation of miR-21 and downregulation of tumor suppressor genes Pdcd4 and Reck.Journal of occupational health · 2021Article
- MicroRNA (miRNA) Differential Expression and Exposure to Crude-Oil- Related Compounds.MicroRNA (Shariqah, United Arab Emirates) · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 2 institutions in 2 countries.
Funding
Abstract
Hexavalent chromium [Cr(VI)] is a well-known human carcinogen associated with an increased risk of lung cancer. However, the mechanisms underlying Cr(VI)-induced carcinogenesis remain unclear. MicroRNA-21 (miR-21) is a key regulator of oncogenic processes. Studies have shown that miR-21 exerts its oncogenic activity by targeting the tumor suppressor gene programmed cell death 4 (PDCD4). The present study examined the role of miR-21-PDCD4 signaling in Cr(VI)-induced cell transformation and tumorigenesis. Results showed that Cr(VI) induces ROS generation in human bronchial epithelial (BEAS-2B) cells. Chronic exposure to Cr(VI) is able to cause malignant transformation in BEAS-2B cells. Cr(VI) caused a significant increase of miR-21 expression associated with an inhibition of PDCD4 expression. Notably, STAT3 transcriptional activation by IL-6 is crucial for the Cr(VI)-induced miR-21 elevation. Stable knockdown of miR-21 or overexpression of PDCD4 in BEAS-2B cells significantly reduced the Cr(VI)-induced cell transformation. Furthermore, the Cr(VI) induced inhibition of PDCD4 suppressed downstream E-cadherin protein expression, but promoted β-catenin/TCF-dependent transcription of uPAR and c-Myc. We also found an increased miR-21 level and decreased PDCD4 expression in xenograft tumors generated with chronic Cr(VI)-exposed BEAS-2B cells. In addition, stable knockdown of miR-21 and overexpression of PDCD4 reduced the tumorogenicity of chronic Cr(VI)-exposed BEAS-2B cells in nude mice. Taken together, these results demonstrate that the miR-21-PDCD4 signaling axis plays an important role in Cr(VI)-induced carcinogenesis.
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.