ArticleMolecular endocrinology (Baltimore, Md.)2011
SGK3 is an estrogen-inducible kinase promoting estrogen-mediated survival of breast cancer cells.
Article in Molecular endocrinology (Baltimore, Md.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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Who cites it
52 citing papers in PubMed, 68 citations in OpenAlex.
- Somatic mutation profiling and associations with prognosis and trastuzumab benefit in early breast cancer.Journal of the National Cancer Institute · 2013Trial
- SGK3 promoter deletion in late-onset hypophosphatemic rickets, a possible genetic cause of the disease.Orphanet journal of rare diseases · 2026Article
- CircKIAA1617 promotes stemness via USP14/PGRMC1-mediated autophagy and lipid metabolism reprogramming in ER-positive breast cancer.Molecular cancer · 2026Article
- Rat somatic genome editing enables ER+ breast cancer modeling.bioRxiv : the preprint server for biology · 2025Article
- Recent Prospectives of Cellular Signaling Role for Mammary Gland Carcinogenesis.Anti-cancer agents in medicinal chemistry · 2025Review
- The SGK3/GSK3β/β-catenin signaling promotes breast cancer stemness and confers resistance to alpelisib therapy.International journal of biological sciences · 2025Article
- Integrative modeling uncovers p21-driven drug resistance and prioritizes therapies for PIK3CA-mutant breast cancer.NPJ precision oncology · 2024Article
- Molecular features of luminal breast cancer defined through spatial and single-cell transcriptomics.Clinical and translational medicine · 2024Article
- Role of inositol polyphosphate-4-phosphatase type II in oncogenesis of digestive system tumors.World journal of gastrointestinal oncology · 2023Review
- ERβ1 Sensitizes and ERβ2 Desensitizes ERα-Positive Breast Cancer Cells to the Inhibitory Effects of Tamoxifen, Fulvestrant and Their Combination with All-Trans Retinoic Acid.International journal of molecular sciences · 2023Article
- AKTIP loss is enriched in ERα-positive breast cancer for tumorigenesis and confers endocrine resistance.Cell reports · 2022Article
- Ontogeny and Vulnerabilities of Drug-Tolerant Persisters in HER2+ Breast Cancer.Cancer discovery · 2022Article
- Contributions of SGK3 to transporter-related diseases.Frontiers in cell and developmental biology · 2022Review
- TRESK Regulates Gm11874 to Induce Apoptosis of Spinal Cord Neurons via ATP5i Mediated Oxidative Stress and DNA Damage.Neurochemical research · 2021Article
- Mechanisms of Resistance to PI3K Inhibitors in Cancer: Adaptive Responses, Drug Tolerance and Cellular Plasticity.Cancers · 2021Review
- Cancer and Stress: Does It Make a Difference to the Patient When These Two Challenges Collide?Cancers · 2021Review
- Amphiregulin retains ERα expression in acquired aromatase inhibitor resistant breast cancer cells.Endocrine-related cancer · 2020Article
- A Brief Overview of the Paradoxical Role of Glucocorticoids in Breast Cancer.Breast cancer : basic and clinical research · 2020Review
- Increased expression of the HDAC9 gene is associated with antiestrogen resistance of breast cancers.Molecular oncology · 2019Article
- Functional roles of lncRNAs and its potential mechanisms in neuropathic pain.Clinical epigenetics · 2019Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Serum- and glucocorticoid-inducible kinase 3 (SGK3) is a protein kinase of the AGC family of protein kinase A, protein kinase G, and protein kinase C and functions downstream of phosphatidylinositol 3-kinase (PI3K). Recent study revealed that SGK3 plays a pivotal role in Akt/protein kinase B independent signaling downstream of oncogenic PI3KCA mutations in breast cancer. Here we report that SGK3 is an estrogen receptor (ER) transcriptional target and promotes estrogen-mediated cell survival of ER-positive breast cancer cells. Through a meta-analysis on 22 microarray studies of breast cancer in the Oncomine database, we found that the expression of SGK3 is significantly higher (5.7-fold, P < 0.001) in ER-positive tumors than in ER-negative tumors. In ER-positive breast cancer cells, SGK3 expression was found to be induced by 17β-estradiol (E(2)) in a dose- and time-dependent manner, and the induction of SGK3 mRNA by E(2) is independent of newly synthesized proteins. We identified two ERα-binding regions at the sgk3 locus through chromatin immunoprecipitation with massively parallel DNA sequencing. Promoter analysis revealed that ERα stimulates the activity of sgk3 promoters by interaction with these two ERα-binding regions on E(2) treatment. Loss-of-function analysis indicated that SGK3 is required for E(2)-mediated cell survival of MCF-7 breast carcinoma cells. Moreover, overexpression of SGK3 could partially protect MCF-7 cells against apoptosis caused by antiestrogen ICI 182,780. Together, our study defines the molecular mechanism of regulation of SGK3 by estrogen/ER and provides a new link between the PI3K pathway and ER signaling as well as a new estrogen-mediated cell survival mechanism mediated by SGK3 in breast cancer cells.
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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.