ArticleTheranostics2017
Tamoxifen activates Nrf2-dependent SQSTM1 transcription to promote endometrial hyperplasia.
Article in Theranostics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 46 citations in OpenAlex.
- Integrative single-cell and bulk transcriptomics define cell death patterns and ZDHHC22 in gastric cancer progression.BMC medical genomics · 2026Article
- Oxidative DNA damage induced by 3,4-diOH-TAM, a tamoxifen metabolite, in relation to endometrial carcinogenesis.Scientific reports · 2025Article
- LncRNA DEPDC1-AS1 drives the progression of endometrial carcinoma by regulating miR-508-3p.Discover oncology · 2025Article
- HACE1 as a bridge between oxidative stress and autophagy.Frontiers in immunology · 2025Review
- Autophagy Involvement in Non-Neoplastic and Neoplastic Endometrial Pathology: The State of the Art with a Focus on Carcinoma.International journal of molecular sciences · 2024Review
- PAQR4 oncogene: a novel target for cancer therapy.Medical oncology (Northwood, London, England) · 2024Review
- Fibroblast growth factor 1 ameliorates thin endometrium in rats through activation of the autophagic pathway.Frontiers in pharmacology · 2023Article
- Article
- The Multifaceted Role of Autophagy in Endometrium Homeostasis and Disease.Reproductive sciences (Thousand Oaks, Calif.) · 2022Review
- The Role of mTOR and eIF Signaling in Benign Endometrial Diseases.International journal of molecular sciences · 2022Review
- Ethanol-Extracted Cameroonian Propolis Counteracts Tamoxifen-Induced Endometrial Hyperplasia by Modulating Apoptosis and Proliferation-Regulating Proteins in the Ovaries of Intact Wistar Rats.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Ferroptosis: Opportunities and Challenges in Treating Endometrial Cancer.Frontiers in molecular biosciences · 2022Review
- Tamoxifen Twists Again: On and Off-Targets in Macrophages and Infections.Frontiers in pharmacology · 2022Review
- CK1δ stimulates ubiquitination-dependent proteasomal degradation of ATF4 to promote chemoresistance in gastric Cancer.Clinical and translational medicine · 2021Article
- Autophagy in the physiological endometrium and cancer.Autophagy · 2021Review
- Sirt1 deacetylates and stabilizes p62 to promote hepato-carcinogenesis.Cell death & disease · 2021Article
- Aqueous Extract ofEvidence-based complementary and alternative medicine : eCAM · 2021Article
- c-MYC-directed NRF2 drives malignant progression of head and neck cancer via glucose-6-phosphate dehydrogenase and transketolase activation.Theranostics · 2021Article
- Targeting ATF4-dependent pro-survival autophagy to synergize glutaminolysis inhibition.Theranostics · 2021Article
- IGF2BP1 overexpression stabilizes PEG10 mRNA in an m6A-dependent manner and promotes endometrial cancer progression.Theranostics · 2021Article
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Long-term application of Tamoxifen (TAM) is usually recommended for hormone receptor positive breast cancer patients. Unfortunately, TAM will inevitably increase the incidence of endometrial hyperplasia even endometrial cancer. Despite of substantial investigations, no effective approaches to prevent TAM-induced endometrial carcinogenesis have been acknowledged. In this study, we found that inhibition of Nrf2 could be valuable to prevent TAM-induced endometrial hyperplasia. Upon TAM treatment, the mRNA and protein expression of autophagy adaptor SQSTM1 was specifically increased in endometrial cells but not breast cancer cells. Knocking-down of SQSTM1 expression retarded TAM-promoted growth of endometrial cancer cells. TAM stimulated SQSTM1 transcription specifically in endometrial cells by enhancing phosphorylation and nuclear translocation of Nrf2. Indeed, the expression of Nrf2 and SQSTM1 were positively correlated in primary endometrial tissues. In rats with TAM-induced endometrial hyperplasia, both Nrf2 and SQSTM1 expression were increased. Nrf2 inhibitor brusatol effectively attenuated TAM-induced SQSTM1 upregulation and endometrial hyperplasia. The kinase of Nrf2, PRKCD, was activated by TAM. Once PRKCD was depleted, TAM failed to promote Nrf2 phosphorylation and SQSTM1 expression. In summary, TAM stimulated Nrf2-dependent SQSTM1 transcription to promote endometrial hyperplasia by activating PRKCD. Therefore, blocking PRKCD-Nrf2-SQSTM1 signaling could be useful to prevent TAM-induced endometrial hyperplasia.
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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.