Evidence map›Paper›PMID 40232565›Full record

ArticleMolecular biology reports2025

FADS2 inhibits colorectal cancer cell proliferation by regulating ferroptosis through SLC7A11/GPX4.

Qinghui Yang, Hao Zhang, Jing Luo, Hongmei Yu, Xiaodi Yang, Chen Wang

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In one paragraph

Article in Molecular biology reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Review
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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

6 authors.

Qinghui Yang *Department of Oncology, Minhang Branch, Zhongshan Hospital, Fudan University, No. 170 Xinsong Road, Minhang District, Shanghai, China.
Hao Zhang *Department of Oncology, Minhang Branch, Zhongshan Hospital, Fudan University, No. 170 Xinsong Road, Minhang District, Shanghai, China.
Jing LuoDepartment of Oncology, Minhang Branch, Zhongshan Hospital, Fudan University, No. 170 Xinsong Road, Minhang District, Shanghai, China.
Hongmei YuDepartment of Oncology, Minhang Branch, Zhongshan Hospital, Fudan University, No. 170 Xinsong Road, Minhang District, Shanghai, China.
Xiaodi YangDepartment of Oncology, Minhang Branch, Zhongshan Hospital, Fudan University, No. 170 Xinsong Road, Minhang District, Shanghai, China. yxiaodi1986@sina.com.
Chen WangDepartment of Oncology, Minhang Branch, Zhongshan Hospital, Fudan University, No. 170 Xinsong Road, Minhang District, Shanghai, China. wang_c@fudan.edu.cn.

Funding

Minhang District Health Committee Project 2023MW65
6 · The paper itself

Abstract

backgroundColorectal cancer (CRC) is a leading factor in cancer mortality globally. Ferroptosis, a regulated cell death described via lipid peroxidation, is crucial in cancer biology. This study explores the link between ferroptosis, FADS2, and CRC, focusing on the prognostic significance and therapeutic potential of targeting FADS2.

methodsThe differential expression analysis of the Cancer Genome Atlas-colon adenocarcinoma (TCGA-COAD) and GSE36400 datasets was conducted to determine key ferroptosis-related genes, followed by functional enrichment analysis. Prognosis-related genes were assessed utilizing Least Absolute Shrinkage and Selection Operator (LASSO) Cox regression. Genetic variation analysis and immune analysis were employed to evaluate the clinical significance of FADS2. The impacts of FADS2 knockdown on CRC cell migration, proliferation, invasion, and ferroptosis were evaluated by in vitro cell experiments.

results64 key ferroptosis-related genes in CRC were highly enriched in pathways such as glutathione metabolism and peroxisome. Eleven prognosis-associated genes were identified, with TP53 showing the highest mutation frequency. High FADS2 expression was linked to poorer prognosis and higher immune cell infiltration. FADS2 knockdown significantly decreased glutathione (GSH) levels, SLC7A11, and GPX4 expression, increased malondialdehyde (MDA) levels, indicating the promotion of ferroptosis. Functional tests revealed knockdown FADS2 repressed CRC cell proliferation, migration, and invasion. SLC7A11 or GPX4 overexpression partially rescued the effects of FADS2 knockdown. Additionally, FADS2 knockdown enhances the chemosensitivity of CRC cells to oxaliplatin.

conclusionFADS2 is essential for encouraging CRC cell proliferation and tumor growth by preventing ferroptosis. Targeting FADS2 may enhance ferroptosis and suppress CRC progression, offering a possible course of treatment for CRC patients. The knockdown of FADS2 enhances the chemosensitivity of CRC cells to oxaliplatin, providing valuable insights for future clinical applications.

Indexed as

Amino Acid Transport System y+Colorectal NeoplasmsFatty Acid DesaturasesFerroptosisPhospholipid Hydroperoxide Glutathione PeroxidaseCell Line, TumorCell MovementCell ProliferationGene Expression Regulation, NeoplasticHumansPrognosisAmino Acid Transport System y+FADS2 protein, humanFatty Acid DesaturasesPhospholipid Hydroperoxide Glutathione PeroxidaseSLC7A11 protein, humanCell proliferationColorectal cancerFADS2FerroptosisPrognosis

Identifiers

PMID40232565

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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.