ReviewHeliyon2024
Cholesterol: The driving force behind the remodeling of tumor microenvironment in colorectal cancer.
Review in Heliyon, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed.
- Oral Metronomic Delivery of Atorvastatin and Docetaxel via Transporter-Targeted Nanoemulsions Enhances Antitumor Efficacy and Immune Modulation in Colon Cancer.Pharmaceutics · 2025Article
- Tumor Microenvironment, Inflammation, and Inflammatory Prognostic Indices in Diffuse Large B-Cell Lymphomas: A Narrative Review.International journal of molecular sciences · 2025Review
- Myeloid-Derived LGALS9-P4HB Immune Interaction Promotes Metastasis in Gastric Cancer Through Enhanced Cell Proliferation and Lipid Metabolism.Journal of cellular and molecular medicine · 2025Article
- Constructing a Prognostic Model for Subtypes of Colorectal Cancer Based on Machine Learning and Immune Infiltration-Related Genes.Journal of cellular and molecular medicine · 2025Article
- Global Research Trends and Hotspots in the Role of Cholesterol in Colorectal Cancer: A Bibliometric Analysis.Human mutation · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Essential membrane components and metabolites with a wide range of biological roles are both produced by cholesterol metabolism. Cell-intrinsic and cell-extrinsic stimuli alter cholesterol metabolism in the tumor microenvironment (TME), which in turn encourages colorectal carcinogenesis. Metabolites produced from cholesterol play intricate roles in promoting the development of colorectal cancer (CRC) and stifling immunological responses. By altering the extracellular matrix of the main tumor, redesigning its immunological environment, and altering its mechanical stiffness, cholesterol can encourage the epithelial-mesenchymal transition of the primary tumor, opening up a pathway for tumor metastasis. Its functions in TME remodeling and tumor prevention have been recently identified. In this review we address the function of cholesterol in TME remodeling and therapeutic techniques designed to block cholesterol metabolism, and discuss how combining these strategies with already available anti-CRC medicines can have combined effects and open up new therapeutic avenues.
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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.