ArticleToxicology and applied pharmacology2015
Cadmium promotes the proliferation of triple-negative breast cancer cells through EGFR-mediated cell cycle regulation.
Article in Toxicology and applied pharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
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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.
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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
15 citing papers in PubMed, 42 citations in OpenAlex.
- Differential Effects of 17β-Estradiol, Its Metabolites, and Cadmium on Cytotoxicity and Redox-Related Pathways in Doxorubicin-Sensitive and -Resistant Breast Cancer Cell Lines.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Multi-Targeted Mechanisms of Phytochemicals in Mitigating Cadmium-Induced Breast Cancer.Medicines (Basel, Switzerland) · 2026Review
- Mechanisms of Heavy Metal Cadmium (Cd)-Induced Malignancy.Biological trace element research · 2025Review
- Cadmium decreases human gingival fibroblast viability and induces pro-inflammatory response associated with Akt and MAPK pathway activation.Frontiers in toxicology · 2025Article
- New triazole-based coordination complexes as antitumor agents against triple negative breast cancer MDA-MB-468 cell line.RSC advances · 2023Article
- Bioinformatics analysis of key genes and potential mechanism in cadmium-induced breast cancer progression.Environmental science and pollution research international · 2022Article
- BST2 promotes growth and induces gefitinib resistance in oral squamous cell carcinoma via regulating the EGFR pathway.Archives of medical science : AMS · 2021Article
- Dietary cadmium chloride impairs shell biomineralization by disrupting the metabolism of the eggshell gland in laying hens.Journal of animal science · 2020Article
- Endocrine disruption through membrane estrogen receptors and novel pathways leading to rapid toxicological and epigenetic effects.The Journal of steroid biochemistry and molecular biology · 2019Review
- Cadmium induces progesterone receptor gene expression via activation of estrogen receptor in human ovarian cancer cells.Research in pharmaceutical sciences · 2018Article
- Suppression of ferroportin expression by cadmium stimulates proliferation, EMT, and migration in triple-negative breast cancer cells.Toxicology and applied pharmacology · 2018Article
- The protective role of melatonin in cadmium-induced proliferation of ovarian cancer cells.Research in pharmaceutical sciences · 2018Article
- Blood cadmium levels associated with short distant metastasis-free survival time in invasive breast cancer.Environmental science and pollution research international · 2017Article
- Cadmium stimulates metastasis-associated phenotype in triple-negative breast cancer cells through integrin and β-catenin signaling.Toxicology and applied pharmacology · 2017Article
- Regulation of therapeutic resistance in cancers by receptor tyrosine kinases.American journal of cancer research · 2016Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Cadmium (Cd) is a carcinogenic metal which is implicated in breast cancer by epidemiological studies. It is reported to promote breast cancer cell growth in vitro through membrane receptors. The study described here examined Cd-mediated growth of non-metastatic human breast cancer derived cells that lack receptors for estrogen, progesterone, and HER2. Treatment of triple-negative HCC 1937 cells with 0.1-0.5 μM Cd increased cell growth by activation of AKT and ERK. Accelerated cell cycle progression was achieved by increasing the levels of cyclins A, B, and E, as well as those of CDKs 1 and 2. Although triple negative cells lack estrogen receptor, they express high levels of EGFR. Therefore, further studies on HCC 1937 and another triple-negative cell line, HCC 38, were conducted using specific siRNA and an inhibitor of EGFR to determine whether EGFR was responsible for mediating the effect of Cd. The results revealed that in both cell types EGFR was not only activated upon Cd treatment, but was also essential for the downstream activation of AKT and ERK. Based on these observations, it is concluded that, in breast cancer cells lacking estrogen receptor, sub-micromolar concentration of Cd can promote cell proliferation. Furthermore, that EGFR plays a critical role in this process.
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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.