Evidence map›Paper›PMID 42067616›Full record

ArticleExperimental & molecular medicine2026

SLC38A4 promotes Kupffer cell phagocytosis and suppresses tumor liver metastasis.

Jie Li, Yong-Da Liu, Renjie Wang, Xing-Yi Lin, Yi-Qing Zhu, Wan-Peng Lu, Yan-Fang Tang, Xing-Peng Guo, Yu-Han Ai, Ting-Ting Xu and 5 more

Abstract read
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In one paragraph

Article in Experimental & molecular medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0cells of the map it votes in
0citing papers in PubMed
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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

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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

15 authors.

Jie Li *Department of Medical Genetics, Shanghai Key Laboratory of Medical Bioprotection, Key Laboratory of Biological Defense, Ministry of Education, Naval Medical University, Shanghai, China.ORCID http://orcid.org/0000-0002-3856-9986
Yong-Da Liu *Department of Medical Genetics, Shanghai Key Laboratory of Medical Bioprotection, Key Laboratory of Biological Defense, Ministry of Education, Naval Medical University, Shanghai, China.
Renjie Wang *Department of Colorectal Surgery, Fudan University Shanghai Cancer Center, Shanghai, China.
Xing-Yi LinDepartment of Medical Genetics, Shanghai Key Laboratory of Medical Bioprotection, Key Laboratory of Biological Defense, Ministry of Education, Naval Medical University, Shanghai, China.
Yi-Qing ZhuDepartment of Medical Genetics, Shanghai Key Laboratory of Medical Bioprotection, Key Laboratory of Biological Defense, Ministry of Education, Naval Medical University, Shanghai, China.
Wan-Peng LuDepartment of Medical Genetics, Shanghai Key Laboratory of Medical Bioprotection, Key Laboratory of Biological Defense, Ministry of Education, Naval Medical University, Shanghai, China.
Yan-Fang TangDepartment of Medical Genetics, Shanghai Key Laboratory of Medical Bioprotection, Key Laboratory of Biological Defense, Ministry of Education, Naval Medical University, Shanghai, China.
Xing-Peng GuoDepartment of Medical Genetics, Shanghai Key Laboratory of Medical Bioprotection, Key Laboratory of Biological Defense, Ministry of Education, Naval Medical University, Shanghai, China.
Yu-Han AiDepartment of Medical Genetics, Shanghai Key Laboratory of Medical Bioprotection, Key Laboratory of Biological Defense, Ministry of Education, Naval Medical University, Shanghai, China.
Ting-Ting XuDepartment of Medical Genetics, Shanghai Key Laboratory of Medical Bioprotection, Key Laboratory of Biological Defense, Ministry of Education, Naval Medical University, Shanghai, China.
Sen LinDepartment of Medical Genetics, Shanghai Key Laboratory of Medical Bioprotection, Key Laboratory of Biological Defense, Ministry of Education, Naval Medical University, Shanghai, China.
Mei HuangDepartment of Medical Genetics, Shanghai Key Laboratory of Medical Bioprotection, Key Laboratory of Biological Defense, Ministry of Education, Naval Medical University, Shanghai, China.
Jinghan WangInstitute of Hepatobiliary and Pancreatic Surgery, Department of Hepatobiliary and Pancreatic Surgery, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai, China. EHHBP@tongji.edu.cn.
Xiao-Ting ZhuDepartment of Anatomy and Physiology, Shanghai Jiao Tong University School of Medicine, Shanghai, China. zhuxiaoting127@shsmu.edu.cn.
Ji-Hang YuanDepartment of Medical Genetics, Shanghai Key Laboratory of Medical Bioprotection, Key Laboratory of Biological Defense, Ministry of Education, Naval Medical University, Shanghai, China. jihangyuan@smmu.edu.cn.ORCID http://orcid.org/0000-0003-1297-7743

Funding

National Natural Science Foundation of China (National Science Foundation of China) 32400761National Natural Science Foundation of China (National Science Foundation of China) 32470973National Natural Science Foundation of China (National Science Foundation of China) 82421005National Natural Science Foundation of China (National Science Foundation of China) 82422059National Natural Science Foundation of China (National Science Foundation of China) 92374119
6 · The paper itself

Abstract

Metastasis is the main cause of cancer-related death. The liver is an organ with high metastatic tropism for various malignancies. Hepatic-resident macrophage Kupffer cells are the major non-parenchymal cells in the liver that phagocytize disseminated tumor cells to restrict liver metastasis. However, the critical molecules that modulate phagocytosis of tumor cells by Kupffer cells are still largely unknown. Here, we identified SLC38A4 expressed on tumor cells as a critical suppressor during tumor liver metastasis. SLC38A4 enhances the phagocytosis of various tumor cells by Kupffer cells, leading to a reduction in liver metastasis. Mechanistically, SLC38A4 downregulates the expression of "don't eat me" molecule CD24, which mediates the roles of SLC38A4 in Kupffer cells phagocytosis and tumor liver metastasis. MYC directly binds to CD24 promoter and activates CD24 transcription. Through downregulating MYC, SLC38A4 suppresses the expression of CD24. Patients with low SLC38A4 expression in tumors have more liver metastases. This study demonstrates that SLC38A4 promotes Kupffer cell phagocytosis and restricts tumor liver metastasis by suppressing CD24. The SLC38A4/MYC/CD24 axis represents a novel phagocytosis checkpoint for Kupffer cells and a potential therapeutic target for liver metastasis.

Indexed as

Kupffer CellsLiver NeoplasmsPhagocytosisAnimalsCD24 AntigenCell Line, TumorGene Expression Regulation, NeoplasticHumansMiceCD24 Antigen

Identifiers

PMID42067616
PMCPMC13234026

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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.