Evidence map›Paper›PMID 42122151›Full record

ArticleCancers2026

Loss of SALL1 Promotes Hepatocellular Carcinoma Growth and Is Associated with Poor Clinical Outcome.

Yoshifumi Saito, Carlos Ichiro Kasano-Camones, Atsumi Tamura, Shioko Kimura, Xiaoting Yu, Yutong Cui, Vorthon Sawaswong, Kristopher W Krausz, Dong Wang, Aijuan Qu and 3 more

Abstract read
In one paragraph

Article in Cancers, 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

13 authors.

Yoshifumi SaitoCancer Innovation Laboratory, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Carlos Ichiro Kasano-CamonesCancer Innovation Laboratory, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.ORCID 0009-0000-6684-7472
Atsumi TamuraCancer Innovation Laboratory, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Shioko KimuraCancer Innovation Laboratory, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Xiaoting YuCancer Innovation Laboratory, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.ORCID 0000-0001-8886-4433
Yutong CuiKey Laboratory of Remodeling-Related Cardiovascular Diseases, Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Capital Medical University, Ministry of Education, Beijing 100069, China.
Vorthon SawaswongCancer Innovation Laboratory, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Kristopher W KrauszCancer Innovation Laboratory, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Dong WangDepartment of General Surgery, Beijing Friendship Hospital, National Clinical Research Center for Digestive Diseases, State Key Laboratory of Digestive Health, Beijing Key Laboratory of Cancer Invasion and Metastasis Research, Capital Medical University, Beijing 100050, China.
Aijuan QuKey Laboratory of Remodeling-Related Cardiovascular Diseases, Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Capital Medical University, Ministry of Education, Beijing 100069, China.ORCID 0000-0001-6661-1953
Yusuke InoueLaboratory of Metabolism, Division of Molecular Science, Graduate School of Science and Technology, Gunma University, Kiryu 376-8515, Gunma, Japan.ORCID 0000-0002-9710-7482
Shogo TakahashiCancer Innovation Laboratory, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Frank J GonzalezCancer Innovation Laboratory, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND/

objectivesHepatocellular carcinoma (HCC) remains a major malignancy with high incidence and mortality, in part due to its diverse etiology and intratumoral heterogeneity, which contributes to drug resistance and frequent recurrence. SALL1 (Spalt-Like Transcription Factor 1), a zinc-finger transcription factor, was reported to function as a tumor suppressor in several cancers, including breast cancer and glioma, and accumulating evidence support its involvement in tumor biology. In this study, the role of SALL1 in HCC was examined.

methodsPublic RNA and protein databases derived from human HCC were interrogated. Western blotting quantification of clinical HCC for SALL1 levels was carried out. Cell culture and xenograft studies were performed using genetically modified HCC tumor cells.

resultsAs revealed by pubic RNA and protein database analysis and further western blotting quantification of clinical samples of HCC, SALL1 is decreased in human HCC. The effect of reduced SALL1 expression on the tumorigenic properties and transcriptional regulation in HCC was then examined. Knockdown of SALL1 in the HCC cell lines Huh7 and Hep3B, enhanced cell proliferation in vitro and accelerated tumor growth in a xenograft mouse model, suggesting that lower SALL1 expression increases cell proliferation and tumorigenesis in HCC. RNA-seq and ChIP analyses further identified three novel candidate target genes (

conclusionsThese findings establish SALL1 as a possible tumor suppressor and provide new insights into the biological significance of SALL1 downregulation in HCC. SALL1 could be a candidate prognostic marker and a potential therapeutic target.

Indexed as

hepatocellular carcinomaHepG2Huh-7SALL1transcription factortumor suppressorxenograft

Identifiers

PMID42122151
PMCPMC13162894

What Socratic holds

Textmetadata
LicenceCC BY
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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.