Evidence map›Paper›PMID 40862287›Full record

ArticleJournal of clinical and translational hepatology2025

ATOX1 Promotes Hepatocellular Carcinoma Carcinogenesis via Activation of the c-Myb/PI3K/AKT Signaling Pathway.

Qin Ouyang, Siyu Jia, Qianyu Zhu, Yanmeng Li, Huaduan Zi, Sisi Chen, Pingping He, Hengcheng Tang, Yanling Li, Anjian Xu and 5 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of clinical and translational hepatology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. Article
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.

Qin OuyangLaboratory of Molecular Biology, Beijing Institute of Clinical Medicine, Beijing Friendship Hospital, Capital Medical University, State Key Laboratory of Digestive Health; National Clinical Research Center for Digestive Diseases, Beijing, China.
Siyu JiaLaboratory of Molecular Biology, Beijing Institute of Clinical Medicine, Beijing Friendship Hospital, Capital Medical University, State Key Laboratory of Digestive Health; National Clinical Research Center for Digestive Diseases, Beijing, China.
Qianyu ZhuLaboratory of Molecular Biology, Beijing Institute of Clinical Medicine, Beijing Friendship Hospital, Capital Medical University, State Key Laboratory of Digestive Health; National Clinical Research Center for Digestive Diseases, Beijing, China.
Yanmeng LiLaboratory of Molecular Biology, Beijing Institute of Clinical Medicine, Beijing Friendship Hospital, Capital Medical University, State Key Laboratory of Digestive Health; National Clinical Research Center for Digestive Diseases, Beijing, China.
Huaduan ZiLaboratory of Molecular Biology, Beijing Institute of Clinical Medicine, Beijing Friendship Hospital, Capital Medical University, State Key Laboratory of Digestive Health; National Clinical Research Center for Digestive Diseases, Beijing, China.
Sisi ChenLaboratory of Molecular Biology, Beijing Institute of Clinical Medicine, Beijing Friendship Hospital, Capital Medical University, State Key Laboratory of Digestive Health; National Clinical Research Center for Digestive Diseases, Beijing, China.
Pingping HeLaboratory of Molecular Biology, Beijing Institute of Clinical Medicine, Beijing Friendship Hospital, Capital Medical University, State Key Laboratory of Digestive Health; National Clinical Research Center for Digestive Diseases, Beijing, China.
Hengcheng TangLaboratory of Molecular Biology, Beijing Institute of Clinical Medicine, Beijing Friendship Hospital, Capital Medical University, State Key Laboratory of Digestive Health; National Clinical Research Center for Digestive Diseases, Beijing, China.
Yanling LiLaboratory of Molecular Biology, Beijing Institute of Clinical Medicine, Beijing Friendship Hospital, Capital Medical University, State Key Laboratory of Digestive Health; National Clinical Research Center for Digestive Diseases, Beijing, China.
Anjian XuLaboratory of Molecular Biology, Beijing Institute of Clinical Medicine, Beijing Friendship Hospital, Capital Medical University, State Key Laboratory of Digestive Health; National Clinical Research Center for Digestive Diseases, Beijing, China.
Bei ZhangLaboratory of Molecular Biology, Beijing Institute of Clinical Medicine, Beijing Friendship Hospital, Capital Medical University, State Key Laboratory of Digestive Health; National Clinical Research Center for Digestive Diseases, Beijing, China.
Xiaomin WangLiver Research Center, Beijing Friendship Hospital, Capital Medical University, State Key Laboratory of Digestive Health; National Clinical Research Center for Digestive Diseases,Beijing, China.
Xiaojuan OuLiver Research Center, Beijing Friendship Hospital, Capital Medical University, State Key Laboratory of Digestive Health; National Clinical Research Center for Digestive Diseases,Beijing, China.
Donghu ZhouLaboratory of Molecular Biology, Beijing Institute of Clinical Medicine, Beijing Friendship Hospital, Capital Medical University, State Key Laboratory of Digestive Health; National Clinical Research Center for Digestive Diseases, Beijing, China.ORCID https://orcid.org/0000-0002-9507-5392
Jian HuangLaboratory of Molecular Biology, Beijing Institute of Clinical Medicine, Beijing Friendship Hospital, Capital Medical University, State Key Laboratory of Digestive Health; National Clinical Research Center for Digestive Diseases, Beijing, China.ORCID https://orcid.org/0000-0002-5180-9833

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background and Aims: Despite advancements in diagnostic and therapeutic strategies, hepatocellular carcinoma (HCC) remains a leading cause of cancer-related mortality. Antioxidant-1 (ATOX1) has been implicated in oncogenic processes across various cancer types; however, its specific role in HCC remains unclear. This study aimed to investigate the function of ATOX1 and its underlying molecular mechanisms in HCC. Methods: Immunohistochemical analysis was conducted to assess ATOX1 expression in HCC tissues. Cell Counting Kit-8, colony formation, Transwell migration, flow cytometry, and reactive oxygen species (ROS) assays were employed to evaluate the malignant behaviors of tumor cells. A xenograft mouse model was employed to assess the effects of ATOX1 knockdown on tumor growth Results: ATOX1 expression was significantly elevated in HCC tumor tissues. ATOX1 promoted cell proliferation, colony formation, and migration. Knockdown of ATOX1 suppressed tumor growth Conclusions: ATOX1 may promote HCC carcinogenesis through the activation of the c-Myb/PI3K/AKT pathway and the inhibition of copper accumulation and oxidative stress.

Indexed as

Antioxidant-1ATOX1c-Myb/PI3K/AKT pathwayCopper transportingHepatocellular carcinomaReactive oxygen species

Identifiers

PMID40862287
PMCPMC12375821

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.