ArticleCell reports2015
Endogenous Sterol Metabolites Regulate Growth of EGFR/KRAS-Dependent Tumors via LXR.
Article in Cell reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
55 citing papers in PubMed, 1 synthesis or guideline pooled it, 83 citations in OpenAlex.
- Cholesterol and Its Derivatives: Multifaceted Players in Breast Cancer Progression.Frontiers in oncology · 2022Pooled it
- NSDHL as a regulator of lipid peroxidation and ER stress-mediated apoptosis in ovarian cancer.Biology direct · 2026Article
- MSMO1 promotes chemotherapy resistance through modulation of T-MAS metabolism via PERK/elF2α/ATF4/CHOP pathway.iScience · 2026Article
- METTL16-mediated mJournal of experimental & clinical cancer research : CR · 2026Article
- Liver X receptor: A potential target for inflammatory bowel disease and colorectal cancer (Review).Molecular medicine reports · 2026Review
- Integrated Bioinformatics Analysis Revealing that the NSDHL Gene Might Be Associated with the Progression of Western HFD/SW-Induced Hepatocellular CarcinomaEndocrine, metabolic & immune disorders drug targets · 2026Article
- USP43 promotes gemcitabine resistance by regulating cholesterol homeostasis through E2F1 stabilization in bladder cancer.Journal of experimental & clinical cancer research : CR · 2025Article
- The role of ATP-binding cassette subfamily G member 1 in tumor progression.Cancer medicine · 2024Review
- The cholesterol biosynthesis enzyme FAXDC2 couples Wnt/β-catenin to RTK/MAPK signaling.The Journal of clinical investigation · 2024Article
- Glioblastomas: Hijacking Metabolism to Build a Flexible Shield for Therapy Resistance.Antioxidants & redox signaling · 2023Review
- Melanoma cells induce dedifferentiation and metabolic changes in adipocytes present in the tumor niche.Cellular & molecular biology letters · 2023Article
- Claudin-4-adhesion signaling drives breast cancer metabolism and progression via liver X receptor β.Breast cancer research : BCR · 2023Article
- Prognosis-related molecular subtyping in head and neck squamous cell carcinoma patients based on glycolytic/cholesterogenic gene data.Cancer cell international · 2023Article
- Article
- Development of SOS1 Inhibitor-Based Degraders to TargetJournal of medicinal chemistry · 2022Article
- Lipid metabolism in tumor microenvironment: novel therapeutic targets.Cancer cell international · 2022Review
- Annexin A6 and NPC1 regulate LDL-inducible cell migration and distribution of focal adhesions.Scientific reports · 2022Article
- Ubiquitous Aberration in Cholesterol Metabolism across Pancreatic Ductal Adenocarcinoma.Metabolites · 2022Article
- CPSF1 positively regulates NSDHL by alternative polyadenylation and promotes gastric cancer progression.American journal of cancer research · 2022Article
- A Novel Prognostic Risk Model for Cervical Cancer Based on Immune Checkpoint HLA-G-Driven Differentially Expressed Genes.Frontiers in immunology · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
Abstract
Meiosis-activating sterols (MAS) are substrates of SC4MOL and NSDHL in the cholesterol pathway and are important for normal organismal development. Oncogenic transformation by epidermal growth factor receptor (EGFR) or RAS increases the demand for cholesterol, suggesting a possibility for metabolic interference. To test this idea in vivo, we ablated Nsdhl in adult keratinocytes expressing KRAS(G12D). Strikingly, Nsdhl inactivation antagonized the growth of skin tumors while having little effect on normal skin. Loss of Nsdhl induced the expression of ATP-binding cassette (ABC) transporters ABCA1 and ABCG1, reduced the expression of low-density lipoprotein receptor (LDLR), decreased intracellular cholesterol, and was dependent on the liver X receptor (LXR) α. Importantly, EGFR signaling opposed LXRα effects on cholesterol homeostasis, whereas an EGFR inhibitor synergized with LXRα agonists in killing cancer cells. Inhibition of SC4MOL or NSDHL, or activation of LXRα by sterol metabolites, can be an effective strategy against carcinomas with activated EGFR-KRAS signaling.
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What OpenQuestion holds
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.