Evidence map›Paper›PMID 39687603›Full record

ArticleJHEP reports : innovation in hepatology2025

ALDH1L2 drives HCC progression through TAM polarization.

Jiajun Li, Chi Zhang, Qingqing Zhou, Qinqin Long, Jiayi Chen, Lili Meng, Wei Tian, Yue Yang, Chao Ge, Yuting Su and 3 more

Abstract read
In one paragraph

Article in JHEP reports : innovation in hepatology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing 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

11 citing papers in PubMed.

  1. Self-Propelled HPB@Lip@AB Nanomotors Ameliorate Dry Eye Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
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  5. Frontiers in immunology · 2026
    Article
  6. 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

13 authors.

Jiajun LiState Key Laboratory of Systems Medicine for Cancer, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Chi ZhangState Key Laboratory of Systems Medicine for Cancer, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Qingqing ZhouState Key Laboratory of Systems Medicine for Cancer, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Qinqin LongDepartment of Pathology, The Affiliated Hospital of Youjiang Medical University for Nationalities, Baise, Guangxi, China.
Jiayi ChenDepartment of Laboratory Medicine, Jiading Branch of Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Lili MengDepartment of Pathology, Zhongshan Hospital, Fudan University, Shanghai, China.
Wei TianState Key Laboratory of Systems Medicine for Cancer, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Yue YangState Key Laboratory of Systems Medicine for Cancer, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Chao GeState Key Laboratory of Systems Medicine for Cancer, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Yuting SuState Key Laboratory of Systems Medicine for Cancer, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Xi-Dai LongDepartment of Pathology, The Affiliated Hospital of Youjiang Medical University for Nationalities, Baise, Guangxi, China.
Jun WuDepartment of Laboratory Medicine, Jiading Branch of Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Hua TianState Key Laboratory of Systems Medicine for Cancer, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background & Aims: Dysregulation of one-carbon metabolism is considered an early hallmark of mitochondrial dysfunction and cancer metabolism. ALDH1L2 belongs to the aldehyde dehydrogenase family and plays an important role in tumor progression. However, little is known about the precise role and underlying mechanisms of ALDH1L2 in hepatocellular carcinoma (HCC). Methods: Immunohistochemistry, western blotting, and immunofluorescence staining were used to evaluate ALDH1L2 expression in HCC samples (n = 90) and cell lines (n = 9). A series of Results: ALDH1L2 upregulation is associated with poor prognosis in HCC (hazard ratio 1.923; 95% confidence interval 1.03-3.59; Conclusions: These findings provide the first evidence indicating that ALDH1L2 is directly involved in tumor progression by interacting with tumor-associated macrophages through the Jak2/STAT3 signaling pathway and that ALDH1L2 may be a target molecule for HCC therapy. Impact and implications: This research highlights that ALDH1L2 could serve as a predictive and prognostic marker in HCC. We found that a positive feedback loop between ALDH1L2 and NRF2 promotes HCC progression by activating the IL-6/Jak2/STAT3 signaling axis and tumor-associated macrophage polarization. In addition, we found that ALDH1L2 knockdown enhances the anti-HCC effect of sorafenib.

Indexed as

ALDH1L2CrosstalkFeedback loopHepatocellular carcinomaProgressionTAM

Identifiers

PMID39687603
PMCPMC11648791

What OpenQuestion holds

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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.