Evidence map›Paper›PMID 38263401›Full record

ArticleCell death discovery2024

Non-alcoholic fatty liver disease promotes liver metastasis of colorectal cancer via fatty acid synthase dependent EGFR palmitoylation.

Chi Zhang, Yue Zhang, Yan Dong, Ruiyang Zi, Yijie Wang, Yanrong Chen, Chengxiang Liu, Junyi Wang, Xuesong Wang, Jianjun Li and 2 more

Open access · goldAbstract read
In one paragraph

Article in Cell death discovery, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
6.8field-weighted citation impact, top 2% of its field
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

26 citing papers in PubMed, 24 citations in OpenAlex.

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  12. Frontiers in pharmacology · 2026
    Article
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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

12 authors at 1 institution in 1 country.

Chi Zhang *Department of Oncology and Southwest Cancer Centre, Southwest Hospital, Third Military Medical University (Army Medical University), 400038, Chongqing, China.
Yue Zhang *Department of Oncology and Southwest Cancer Centre, Southwest Hospital, Third Military Medical University (Army Medical University), 400038, Chongqing, China.
Yan Dong *Department of Oncology and Southwest Cancer Centre, Southwest Hospital, Third Military Medical University (Army Medical University), 400038, Chongqing, China.
Ruiyang ZiDepartment of Oncology and Southwest Cancer Centre, Southwest Hospital, Third Military Medical University (Army Medical University), 400038, Chongqing, China.
Yijie WangDepartment of Oncology and Southwest Cancer Centre, Southwest Hospital, Third Military Medical University (Army Medical University), 400038, Chongqing, China.
Yanrong ChenDepartment of Oncology and Southwest Cancer Centre, Southwest Hospital, Third Military Medical University (Army Medical University), 400038, Chongqing, China.
Chengxiang LiuDepartment of Oncology and Southwest Cancer Centre, Southwest Hospital, Third Military Medical University (Army Medical University), 400038, Chongqing, China.
Junyi WangDepartment of Oncology and Southwest Cancer Centre, Southwest Hospital, Third Military Medical University (Army Medical University), 400038, Chongqing, China.
Xuesong WangDepartment of Oncology and Southwest Cancer Centre, Southwest Hospital, Third Military Medical University (Army Medical University), 400038, Chongqing, China.
Jianjun LiDepartment of Oncology and Southwest Cancer Centre, Southwest Hospital, Third Military Medical University (Army Medical University), 400038, Chongqing, China. jianjunli@tmmu.edu.cn.
Houjie LiangDepartment of Oncology and Southwest Cancer Centre, Southwest Hospital, Third Military Medical University (Army Medical University), 400038, Chongqing, China. lianghoujie@sina.com.
Juanjuan OuDepartment of Oncology and Southwest Cancer Centre, Southwest Hospital, Third Military Medical University (Army Medical University), 400038, Chongqing, China. ojj521000@sina.com.ORCID http://orcid.org/0000-0002-4658-246X
Army Medical University · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) 81874072
6 · The paper itself

Abstract

Liver metastasis is the major reason for most of colorectal cancer (CRC) related deaths. Accumulating evidence indicates that CRC patients with non-alcoholic fatty liver disease (NAFLD) are at a greater risk of developing liver metastasis. With the growing prevalence of NAFLD, a better understanding of the molecular mechanism in NAFLD-driven CRC liver metastasis is needed. In this study, we demonstrated that NAFLD facilitated CRC liver metastasis as a metabolic disorder and promoted the stemness of metastatic CRC cells for their colonization and outgrowth in hepatic niches. Metabolically, the lipid-rich microenvironment in NAFLD activated de novo palmitate biosynthesis in metastatic CRC cells via upregulating fatty acid synthase (FASN). Moreover, increased intracellular palmitate bioavailability promoted EGFR palmitoylation to enhance its protein stability and plasma membrane localization. Furthermore, we demonstrated that the FDA-approved FASN inhibitor orlistat could reduce NAFLD-activated endogenous palmitate production, thus inhibiting palmitoylation of EGFR to suppress CRC cell stemness and restrict liver metastasis in synergy with conventional chemotherapy. These findings reveal that the NAFLD metabolic microenvironment boosts endogenous palmitate biosynthesis in metastatic CRC cells and promotes cell stemness via EGFR palmitoylation, and FASN inhibitor orlistat could be a candidate adjuvant drug to suppress liver metastasis in CRC patients with NAFLD.

Identifiers

PMID38263401
PMCPMC10805926
OpenAlexW4391124959

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.