Evidence map›Paper›PMID 41866501›Full record

ArticleCell communication and signaling : CCS2026

Atorvastatin promotes lipid catabolism in colorectal cancer via FDFT1‒mediated inhibition of the PI3K/AKT pathway.

Jiale Xu, Xiaoyu Qin, Longying Xiong, Cheng Zhao, Dan Ge, Yanping Wu, Yixuan Shen, Mengli Yang, Bihan Shen, Min Chen and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell communication and signaling : CCS, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors.

Jiale XuDepartment of Gastroenterology, Affiliated Hospital of Medical School, Nanjing Drum Tower Hospital, Nanjing University of Chinese Medicine, Nanjing City, 210008, Jiangsu Province, P.R. China.
Xiaoyu QinDepartment of Gastroenterology, Affiliated Hospital of Medical School, Nanjing Drum Tower Hospital, Nanjing University of Chinese Medicine, Nanjing City, 210008, Jiangsu Province, P.R. China.
Longying XiongDepartment of Gastroenterology, Affiliated Hospital of Medical School, Nanjing Drum Tower Hospital, Nanjing University, Nanjing City, 210008, Jiangsu Province, P.R. China.
Cheng ZhaoDepartment of Gastroenterology, Affiliated Hospital of Medical School, Nanjing Drum Tower Hospital, Nanjing University, Nanjing City, 210008, Jiangsu Province, P.R. China.
Dan GeDepartment of Gastroenterology, Affiliated Hospital of Medical School, Nanjing Drum Tower Hospital, Nanjing University, Nanjing City, 210008, Jiangsu Province, P.R. China.
Yanping WuDepartment of Gastroenterology, Affiliated Hospital of Medical School, Nanjing Drum Tower Hospital, Nanjing University, Nanjing City, 210008, Jiangsu Province, P.R. China.
Yixuan ShenDepartment of Gastroenterology, Affiliated Hospital of Medical School, Nanjing Drum Tower Hospital, Nanjing University, Nanjing City, 210008, Jiangsu Province, P.R. China.
Mengli YangDepartment of Gastroenterology, Affiliated Hospital of Medical School, Nanjing Drum Tower Hospital, Nanjing University, Nanjing City, 210008, Jiangsu Province, P.R. China.
Bihan ShenDepartment of Gastroenterology, Affiliated Hospital of Medical School, Nanjing Drum Tower Hospital, Nanjing University, Nanjing City, 210008, Jiangsu Province, P.R. China.
Min ChenDepartment of Gastroenterology, Affiliated Hospital of Medical School, Nanjing Drum Tower Hospital, Nanjing University of Chinese Medicine, Nanjing City, 210008, Jiangsu Province, P.R. China.
Chen MinDepartment of Gastroenterology, Affiliated Hospital of Medical School, Nanjing Drum Tower Hospital, Nanjing University of Chinese Medicine, Nanjing City, 210008, Jiangsu Province, P.R. China. croweminchan@nju.edu.cn.

Funding

Nanjing Drum Tower Hospital Young Talent Cultivation Program HA9830202201National Natural Science Foundation of China 8250072869Natural Science Foundation of Jiangsu Province BK20230142
6 · The paper itself

Abstract

As a hydroxymethylglutaryl‒coenzyme A reductase (HMGCR) inhibitors, atorvastatin (ATST) has garnered widespread attention because of its antitumor effects. However, its specific mechanism of action remains incompletely understood. In our study, ATST was found to inhibit AOM/DSS‒induced colorectal cancer (CRC) progression in mice. Mechanistically, by inhibiting HMGCR and depleting cellular cholesterol, ATST activates the SREBP2‒FDFT1 axis. This in turn inhibits the PI3K/AKT pathway, inducing endoplasmic reticulum (ER) stress and autophagy while concurrently promoting lipid catabolism to drive ferroptosis. This study elucidates the mechanism through which ATST regulates lipid catabolism to influence CRC progression, providing a new direction for CRC therapy.

Indexed as

AtorvastatinColorectal NeoplasmsLipid MetabolismPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionAnimalsAutophagyCell Line, TumorEndoplasmic Reticulum StressHumansMiceSterol Regulatory Element Binding Protein 2AtorvastatinPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSterol Regulatory Element Binding Protein 2AtorvastatinColorectal cancerER stressFDFT1Lipid catabolismPI3K/AKT pathway

Identifiers

PMID41866501
PMCPMC13134328

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.