ArticleCancer cell international2026
Squalene synthase induces ERα expression via cholesterol supplementation to confer statin resistance in lung cancer cells.
Article in Cancer cell international, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
backgroundSterol regulatory element-binding proteins (SREBPs) are master regulators of cholesterol and lipid biosynthesis - pathways increasingly linked to cancer progression. Statins, which inhibit HMG-CoA reductase to lower cholesterol, have shown potential in reducing cancer recurrence. However, their efficacy in lung cancer remains uncertain, and predictive biomarkers for statin responsiveness are still lacking.
methodsWe examined the relationship between cholesterol biosynthesis and estrogen receptor alpha (ERα) signaling and assessed the therapeutic potential of targeting this axis in lung cancer models.
resultsOverexpression of farnesyl-diphosphate farnesyltransferase 1 (FDFT1), also known as squalene synthase (SQS), significantly increased the IC50 of lovastatin in lung cancer cell lines, indicating a role in mediating statin resistance. Gene expression profiling revealed enrichment of estrogen receptor alpha (ERα) signaling in SQS-overexpressing cells. Immunohistochemical analysis of 125 NSCLC patient samples showed a positive correlation between SQS and ERα protein expression, and their co-expression was significantly associated with poorer disease-free survival. Mechanistically, SQS upregulated ERα at the protein level via cholesterol replenishment, without altering ESR1 mRNA levels, suggesting a post-transcriptional regulatory mechanism.
conclusionSQS promotes statin resistance in lung cancer by stabilizing ERα through cholesterol replenishment. Its co-expression with ERα predicts poor prognosis, highlighting the SQS–ERα axis as a potential therapeutic target and biomarker for stratifying patients likely to benefit from statin–antiestrogen combination therapy.
Indexed as
Identifiers
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.