ArticleCell death & disease2021
Fatostatin reverses progesterone resistance by inhibiting the SREBP1-NF-κB pathway in endometrial carcinoma.
Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 58 citations in OpenAlex.
- Metabolic Targeting of SREBP1 Reprograms the Obesity-Driven Ascites Immune Microenvironment and Enhances Chemotherapy Response in Obesity-Associated Ovarian Cancer.bioRxiv : the preprint server for biology · 2026Article
- sPLAScience advances · 2026Article
- SREBP2 regulates CCDC25 expression and promotes tumor metastasis in Triple-Negative Breast Cancer.Oncogenesis · 2026Article
- Cancer-associated fibroblasts as key regulators of lipid metabolism in the tumour microenvironment.Oncogene · 2026Review
- Construction and initial validation of key gene network for progesterone resistance in endometrial cancer based on genome-wide CRISPR screening.Scientific reports · 2026Article
- The emerging role of cholesterol metabolism in gynecologic cancer development and therapy.Apoptosis : an international journal on programmed cell death · 2026Review
- CRL4International journal of biological sciences · 2026Article
- Inhibition of Tumor Lipogenesis and Growth by Peptide-Based Targeting of SREBP Activation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- FOXA2 sensitizes endometrial carcinoma to progestin-mediated conservative therapy by triggering PR transcriptional activation.Oncogene · 2025Article
- Hepatocyte nuclear factors dynamically regulate triglyceride metabolic reprogramming in metabolic dysfunction-associated steatotic liver disease: Mechanisms and implications.World journal of hepatology · 2025Review
- Article
- Ferroptosis as a therapeutic target in glioblastoma: Mechanisms and emerging strategies.Molecular therapy. Nucleic acids · 2025Review
- Advances in the molecular mechanisms underlying progestin resistance in endometrial cancer.Fundamental research · 2025Review
- Targeting mitochondria and programmed cell death as potential interventions for metastatic castration-resistant prostate cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025Review
- Review
- Molecular mechanism of tumor-infiltrating immune cells regulating endometrial carcinoma.Genes & diseases · 2025Review
- The Role of Cholesterol Metabolism and Its Regulation in Tumor Development.Cancer medicine · 2025Review
- Oxidative Stress and Reprogramming of Lipid Metabolism in Cancers.Antioxidants (Basel, Switzerland) · 2025Review
- Impaired RelA signaling and lipid metabolism dysregulation in hepatocytes: driving forces in the progression of metabolic dysfunction-associated steatotic liver disease.Cell death discovery · 2025Article
- Canagliflozin alleviates progestin resistance by suppressing RARβ/CRABP2 signaling in THRB knockout endometrial cancer cells.Frontiers in pharmacology · 2025Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Progesterone resistance can significantly restrict the efficacy of conservative treatment for patients with endometrial cancer who wish to preserve their fertility or those who suffer from advanced and recurrent cancer. SREBP1 is known to be involved in the occurrence and progression of endometrial cancer, although the precise mechanism involved remains unclear. In the present study, we carried out microarray analysis in progesterone-sensitive and progesterone-resistant cell lines and demonstrated that SREBP1 is related to progesterone resistance. Furthermore, we verified that SREBP1 is over-expressed in both drug-resistant tissues and cells. Functional studies further demonstrated that the inhibition of SREBP1 restored the sensitivity of endometrial cancer to progesterone both in vitro and in vivo, and that the over-expression of SREBP1 promoted resistance to progesterone. With regards to the mechanism involved, we found that SREBP1 promoted the proliferation of endometrial cancer cells and inhibited their apoptosis by activating the NF-κB pathway. To solve the problem of clinical application, we found that Fatostatin, an inhibitor of SREBP1, could increase the sensitivity of endometrial cancer to progesterone and reverse progesterone resistance by inhibiting SREBP1 both in vitro and in vivo. Our results highlight the important role of SREBP1 in progesterone resistance and suggest that the use of Fatostatin to target SREBP1 may represent a new method to solve progesterone resistance in patients with endometrial cancer.
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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.