ArticleOncogenesis2020
Chronic exposure to cadmium induces a malignant transformation of benign prostate epithelial cells.
Article in Oncogenesis, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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The trial behind it
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Who cites it
24 citing papers in PubMed, 42 citations in OpenAlex.
- Potential Activity of Non-Platinum Metal-Based Organic Complexes Against Different Cancer Cell Types.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Endocrine-disrupting properties of heavy metal exposure contribute to the intergenerational effects on learning and memory.Frontiers in endocrinology · 2026Review
- DNA damage response inhibition is an early event in cadmium-induced breast carcinogenesis.Toxicology and applied pharmacology · 2025Article
- Multivariate Statistical Evaluation of 20 Metals/Metalloid Levels in the Serum of Patients with Prostate Gland Diseases.Indian journal of clinical biochemistry : IJCB · 2025Article
- Research progress on circular RNA in the regulation of drug resistance in genitourinary cancers.Cellular and molecular life sciences : CMLS · 2025Review
- Mechanistic role of metal-responsive transcription factor-1 (MTF1) in cadmium-induced prostate carcinogenesis.International journal of biological sciences · 2025Article
- Cadmium decreases human gingival fibroblast viability and induces pro-inflammatory response associated with Akt and MAPK pathway activation.Frontiers in toxicology · 2025Article
- Anti-Stemness and Anti-Proliferative Effects of Cadmium on Bovine Mammary Epithelial Cells.Veterinary sciences · 2024Article
- The Role of Trace Metals in the Development and Progression of Prostate Cancer.International journal of molecular sciences · 2024Review
- The interplay of miRNAs and ferroptosis in diseases related to iron overload.Apoptosis : an international journal on programmed cell death · 2024Review
- Cadmium-induced Carcinogenesis in Respiratory Organs and the Prostate: Insights from Three Perspectives on Toxicogenomic Approach.Journal of cancer prevention · 2023Review
- ZIC2 induces pro-tumor macrophage polarization in nasopharyngeal carcinoma by activating the JUNB/MCSF axis.Cell death & disease · 2023Article
- Molecular interplay between NOX1 and autophagy in cadmium-induced prostate carcinogenesis.Free radical biology & medicine · 2023Article
- Article
- Urolithin A analog inhibits castration-resistant prostate cancer by targeting the androgen receptor and its variant, androgen receptor-variant 7.Frontiers in pharmacology · 2023Article
- A small molecule inhibitor of Notch1 modulates stemness and suppresses breast cancer cell growth.Frontiers in pharmacology · 2023Article
- Cadmium: A Focus on the Brown Crab (Toxics · 2022Review
- Population-Level Patterns of Prostate Cancer Occurrence: Disparities in Virginia.Current molecular biology reports · 2022Article
- Chronic Leptin Treatment Induces Epithelial-Mesenchymal Transition in MCF10A Mammary Epithelial Cells.Journal of mammary gland biology and neoplasia · 2022Article
- The role of autophagy in metal-induced urogenital carcinogenesis.Seminars in cancer biology · 2021Review
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Epidemiological evidence suggests that cadmium (Cd) is one of the causative factors of prostate cancer, but the effect of Cd on benign prostatic hyperplasia (BPH) remains unclear. This study aimed to determine whether Cd exposure could malignantly transform BPH1 cells and, if so, to dissect the mechanism of action. We deciphered the molecular signaling responsible for BPH1 transformation via RNA-sequencing and determined that Cd induced the expression of zinc finger of the cerebellum 2 (ZIC2) in BPH1 cells. We noted Cd exposure increased ZIC2 expression in the Cd-transformed BPH1 cells that in turn promoted anchorage-independent spheroids and increased expression of stem cell drivers, indicating their role in stem cell renewal. Subsequent silencing of ZIC2 expression in transformed cells inhibited spheroid formation, stem cell marker expression, and tumor growth in nude mice. At the molecular level, ZIC2 interacts with the glioma-associated oncogene family (GLI) zinc finger 1 (GLI1), which activates prosurvival factors (nuclear factor NFκB, B-cell lymphoma-2 (Bcl2), as well as an X-linked inhibitor of apoptosis protein (XIAP)) signaling in Cd-exposed BPH1 cells. Conversely, overexpression of ZIC2 in BPH1 cells caused spheroid formation confirming the oncogenic function of ZIC2. ZIC2 activation and GLI1 signaling induction by Cd exposure in primary BPH cells confirmed the clinical significance of this oncogenic function. Finally, human BPH specimens had increased ZIC2 versus adjacent healthy tissues. Thus, we report direct evidence that Cd exposure induces malignant transformation of BPH via activation of ZIC2 and GLI1 signaling.
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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.