Evidence map›Paper›PMID 40697225›Full record

ArticleWorld journal of gastrointestinal oncology2025

SAC3 domain containing 1 intervention in energy metabolism reprogramming assists in the progression of hepatocellular carcinoma.

Xue-Jing Lin, Er-Jiang Tang, Bin Sun, Ai-Li Wang, Ying Chen, Lei Chen, Yi-Yang Xue, A-Jian Li, Chun-Ying Liu

Abstract read
In one paragraph

Article in World journal of gastrointestinal oncology, 2025. 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

9 authors.

Xue-Jing LinCenter for Clinical Research and Translational Medicine, Yangpu Hospital, Tongji University School of Medicine, Shanghai 200090, China.
Er-Jiang TangCenter for Clinical Research and Translational Medicine, Yangpu Hospital, Tongji University School of Medicine, Shanghai 200090, China.
Bin SunCenter for Clinical Research and Translational Medicine, Yangpu Hospital, Tongji University School of Medicine, Shanghai 200090, China.
Ai-Li WangCenter for Clinical Research and Translational Medicine, Yangpu Hospital, Tongji University School of Medicine, Shanghai 200090, China.
Ying ChenCenter for Clinical Research and Translational Medicine, Yangpu Hospital, Tongji University School of Medicine, Shanghai 200090, China.
Lei ChenCenter for Clinical Research and Translational Medicine, Yangpu Hospital, Tongji University School of Medicine, Shanghai 200090, China.
Yi-Yang XueDepartment of Chemistry and Biochemistry, University of California, Santa Barbara, Santa Barbara, CA 93106, United States.
A-Jian LiDepartment of General Surgery, Yangpu Hospital, Tongji University School of Medicine, Shanghai 200090, China.
Chun-Ying LiuNational Center for Liver Cancer, Naval Medical University, Shanghai 201805, China. cyliu@sibcb.ac.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMetabolic dysregulation is considered a significant hallmark of hepatocellular carcinoma (HCC). SAC3 domain containing 1 (SAC3D1) functions in the cell cycle, and its expression is upregulated in various cancers. It is known that metabolic changes occur at different stages of the cell cycle to maintain the biosynthesis and replication of both normal and cancer cells. Based on the role of SAC3D1 in mitosis, we hypothesize that abnormal expression of SAC3D1 may affect cellular metabolism. However, it remains unclear whether SAC3D1 mediates the progression of HCC by regulating metabolic reprogramming.

aimTo comprehensively elucidate the impact and molecular mechanism of SAC3D1 on the progression of HCC by regulating the metabolic reprogramming.

methodsThe constructed SAC3D1 overexpression and knockdown HCC cell lines were used for detecting cell proliferation, migration capabilities, as well as glycolysis and adenosine triphosphate (ATP) production rate assays. They were also employed for examining molecular markers associated with cell migration and glycolysis. The transcriptome sequencing data of cells have revealed the pathways potentially influenced by SAC3D1.The tail vein metastasis model and xenograft tumor experiments were utilized to demonstrate SAC3D1's tumor-promoting effects

resultsSAC3D1 expression was upregulated and associated with poor prognosis in HCC patients. SAC3D1 enhanced the proliferation and migration abilities and reduced the population dependence of HCC cells

conclusionThis study found that SAC3D1 enhances HCC cell glycolysis and ATP production

Indexed as

Adenosine triphosphate productionGlycolysisHepatocellular carcinomaMetabolic reprogrammingSAC3 domain containing 1β-Catenin/c-Myc axis

Identifiers

PMID40697225
PMCPMC12278251

What Socratic holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

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.