Tamoxifen-Dependent Induction of AGR2 Is Associated with Increased Aggressiveness of Endometrial Cancer Cells
Language English Country England, Great Britain Media print-electronic
Document type Journal Article
- Keywords
- AGR2, Breast cancer, Endometrial cancer, Tamoxifen,
- MeSH
- Adenocarcinoma chemically induced genetics metabolism pathology MeSH
- A549 Cells MeSH
- Endometrium drug effects metabolism pathology MeSH
- Antineoplastic Agents, Hormonal toxicity MeSH
- Neoplasm Invasiveness MeSH
- Humans MeSH
- MCF-7 Cells MeSH
- Mucoproteins MeSH
- Cell Transformation, Neoplastic chemically induced genetics metabolism pathology MeSH
- Endometrial Neoplasms chemically induced genetics metabolism pathology MeSH
- Oncogene Proteins MeSH
- Cell Movement drug effects MeSH
- Cell Proliferation drug effects MeSH
- Proteins genetics metabolism MeSH
- Retrospective Studies MeSH
- Risk Factors MeSH
- RNA Interference MeSH
- Signal Transduction drug effects MeSH
- Tamoxifen toxicity MeSH
- Transfection MeSH
- Up-Regulation MeSH
- Check Tag
- Humans MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
- Names of Substances
- AGR2 protein, human MeSH Browser
- Antineoplastic Agents, Hormonal MeSH
- Mucoproteins MeSH
- Oncogene Proteins MeSH
- Proteins MeSH
- Tamoxifen MeSH
Tamoxifen treatment in breast cancer patients is associated with increased risk of endometrial malignancies. Significantly, higher AGR2 expression was found in endometrial cancers that developed in women previously treated with tamoxifen compared to those who had not been exposed to tamoxifen. An association of elevated AGR2 level with myometrial invasion occurrence and invasion depth was also found. In vitro analyses identified a stimulatory effect of AGR2 on cellular proliferation. Although adverse tamoxifen effects on endometrial cells remain elusive, our work identifies elevated AGR2 as a candidate tamoxifen-dependent mechanism of action responsible for increased incidence of endometrial cancer.
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