ArticleCurrent medicinal chemistry2026
The Impact of IGFBP6 Knockdown on Cholesterol Metabolism in Breast Cancer Cells.
Article in Current medicinal chemistry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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
3 citing papers in PubMed.
- Review
- Revisiting the Lipid-Cancer Axis: PCSK9, ANGPTL3, and CETP as Emerging Biomarkers and Therapeutic Targets in Oncology.Biomolecules · 2026Review
- Lipid metabolism reprogramming: key mechanism of breast cancer endocrine therapy resistance.Frontiers in oncology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionCholesterol plays a key role in maintaining tumor cell homeostasis. Reduced IGFBP6 expression is associated with an increased risk of breast cancer recurrence. Previous studies showed that IGFBP6 knockdown decreases cholesterol levels in the MDA-MB-231 cell line. This study aimed to investigate how IGFBP6 influences genes involved in cholesterol metabolism.
methodsWe used MDA-MB-231 breast cancer cells with IGFBP6 knockdown. Transcriptomic and proteomic analyses were performed, with selected gene expression validated by RT-PCR. Correlations between IGFBP6 and cholesterol-related genes were evaluated using public RNA-seq datasets.
resultsIGFBP6 knockdown in MDA-MB-231 cells resulted in a threefold decrease in low-density lipoprotein receptor (LDLR) expression and a twofold reduction in LDLR adaptor protein (LDLRAP1) mRNA levels, both responsible for exogenous cholesterol uptake. Meanwhile, PCSK9 expression increased 11-fold (p-adj = 1.4E-93), further limiting uptake. Despite the upregulation of genes involved in endogenous cholesterol synthesis (HMGCS1, HMGCR, FDFT1, SQLE, DHCR24), total cholesterol content in knockdown cells decreased, leading to activation of the sterol-dependent transcription factor SREBF1 (OR = 6.44; p-adj = 0.036). Correlation analysis revealed a significant association between IGFBP6 expression and cholesterol synthesis genes in basal-like breast cancer. DISCUSSION: The altered expression profile of multiple cholesterol metabolism-related genes with known prognostic value aligns with a transcriptional program typical of poor-outcome basal-like tumors. These findings support the role of IGFBP6 as a regulator of lipid metabolism and a potential biomarker for therapeutic stratification.
conclusionThe results of this study indicate that the reduction in cholesterol levels observed in breast cancer cells following IGFBP6 knockdown is primarily due to decreased exogenous uptake. These findings highlight the role of IGFBP6 in regulating cholesterol metabolism and further explain its clinical significance in predicting breast cancer recurrence and progression.
Indexed as
Identifiers
40947699What Socratic 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 Socratic graph.