ArticleBritish journal of cancer2017
Inhibition of autophagy prevents cadmium-induced prostate carcinogenesis.
Article in British journal of cancer, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.
- Heavy metal carcinogenicity: a scoping review of observational & experimental evidence.Frontiers in oncology · 2025Pooled it
- Psoralidin inhibits stemness-associated characteristics in cervical cancer cells via modulation of Oct4/Sox2 expression.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- 5'-Methylthioadenosine Metabolic Reprogramming Drives H3K79 Monomethylation-Mediated PAK2 Upregulation to Promote Cadmium-Induced Breast Cancer Progression by Impairing Autophagic Flux.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Mechanisms of Heavy Metal Cadmium (Cd)-Induced Malignancy.Biological trace element research · 2025Review
- The dynamic face of cadmium-induced Carcinogenesis: Mechanisms, emerging trends, and future directions.Current research in toxicology · 2024Review
- Psoralidin inhibits osteosarcoma growth and metastasis by downregulating ITGB1 expression via the FAK and PI3K/Akt signaling pathways.Chinese medicine · 2023Article
- Article
- Unboxing the molecular modalities of mutagens in cancer.Environmental science and pollution research international · 2022Review
- Carcinogenic Risk of Pb, Cd, Ni, and Cr and Critical Ecological Risk of Cd and Cu in Soil and Groundwater around the Municipal Solid Waste Open Dump in Central Thailand.Journal of environmental and public health · 2022Article
- The role of autophagy in metal-induced urogenital carcinogenesis.Seminars in cancer biology · 2021Review
- Psoralidin prevents caffeine-induced damage and abnormal differentiation of bone marrow mesenchymal stem cells via the classical estrogen receptor pathway.Annals of translational medicine · 2021Article
- Exposure to cadmium and copper triggers cytotoxic effects and epigenetic changes in human colorectal carcinoma HT-29 cells.Experimental and therapeutic medicine · 2021Article
- Role of the PI3K/Akt pathway in cadmium induced malignant transformation of normal prostate epithelial cells.Toxicology and applied pharmacology · 2020Article
- Activation of the Erk/MAPK signaling pathway is a driver for cadmium induced prostate cancer.Toxicology and applied pharmacology · 2020Article
- Chronic exposure to cadmium induces a malignant transformation of benign prostate epithelial cells.Oncogenesis · 2020Article
- Pharmacological Activities of Psoralidin: A Comprehensive Review of the Molecular Mechanisms of Action.Frontiers in pharmacology · 2020Review
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
backgroundCadmium, an established carcinogen, is a risk factor for prostate cancer. Induction of autophagy is a prerequisite for cadmium-induced transformation and metastasis. The ability of Psoralidin (Pso), a non-toxic, orally bioavailable compound to inhibit cadmium-induced autophagy to prevent prostate cancer was investigated.
methodsPsoralidin was studied using cadmium-transformed prostate epithelial cells (CTPE), which exhibit high proliferative, invasive and colony forming abilities. Gene and protein expression were evaluated by qPCR, western blot, immunohistochemistry and immunofluorescence. Xenograft models were used to study the chemopreventive effects in vivo.
resultsCadmium-transformed prostate epithelial cells were treated with Pso resulting in growth inhibition, without causing toxicity to normal prostate epithelial cells (RWPE-1). Psoralidin-treatment of CTPE cells inhibited the expression of Placenta Specific 8, a lysosomal protein essential for autophagosome and autolysosome fusion, which resulted in growth inhibition. Additionally, Pso treatment caused decreased expression of pro-survival signalling proteins, NFκB and Bcl2, and increased expression of apoptotic genes. In vivo, Pso effectively suppressed CTPE xenografts growth, without any observable toxicity. Tumours from Pso-treated animals showed decreased autophagic morphology, mesenchymal markers expression and increased epithelial protein expression.
conclusionsThese results confirm that inhibition of autophagy by Pso plays an important role in the chemoprevention of cadmium-induced prostate carcinogenesis.
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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.