ArticleClinical and translational medicine2020
Tamoxifen induces fatty liver disease in breast cancer through the MAPK8/FoxO pathway.
Article in Clinical and translational medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 7 papers.
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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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Who cites it
7 citing papers in PubMed, 18 citations in OpenAlex.
- Multi-omic analysis of the liver-breast axis reveals key hepatic mediators of breast cancer progression.Science China. Life sciences · 2026Review
- Probing the molecular mechanism of kaempferol in relieving rheumatoid arthritis based on network pharmacology.Scientific reports · 2025Article
- (Pharmaceuticals (Basel, Switzerland) · 2025Article
- Value of negatively correlated miR-205-5p/Cancer pathogenesis and therapy · 2023Article
- Identification of monotonically expressed long non-coding RNA signatures for breast cancer using variational autoencoders.PloS one · 2023Article
- Analysis of Breast Cancer Based on the Dysregulated Network.Frontiers in genetics · 2022Article
- Tamoxifen induces fatty liver disease in breast cancer through the MAPK8/FoxO pathway.Clinical and translational medicine · 2020Article
Corrections and comments
- Erratum issued
Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
backgroundPrevention of metabolic complications of long-term adjuvant endocrine therapy in breast cancers remained a challenge. We aimed to investigate the molecular mechanism in the development of tamoxifen (TAM)-induced fatty liver in both estrogen receptor (ER)-positive and ER-negative breast cancer. METHODS AND
resultsFirst, the direct protein targets (DPTs) of TAM were identified using DrugBank5.1.7. We found that mitogen-activated protein kinase 8 (MAPK8) was one DPT of TAM. We identified significant genes in breast cancer and fatty liver disease (FLD) using the MalaCards human disease database. Next, we analyzed the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways of those significant genes in breast cancer and FLD using the Search Tool for the Retrieval of Interacting Genes/Proteins (STRING). We found that overlapping KEGG pathways in these two diseases were MAPK signaling pathway, Forkhead box O (FoxO) signaling pathway, HIF-1 signaling pathway, AGE-RAGE signaling pathway in diabetic complications, and PI3K-Akt signaling pathway. Furthermore, the KEGG Mapper showed that the MAPK signaling pathway was related to the FoxO signaling pathway. Finally, the functional relevance of breast cancer and TAM-induced FLD was validated by Western blot analysis. We verified that TAM may induce fatty liver in breast cancer through the MAPK8/FoxO signaling pathway.
conclusionBioinformatics analysis combined with conventional experiments may improve our understanding of the molecular mechanisms underlying side effects of cancer drugs, thereby making this method a new paradigm for guiding future studies on this issue.
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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.