Evidence map›Paper›PMID 31802891›Full record

ArticleOncoTargets and therapy2019

NCAPG Promotes The Proliferation Of Hepatocellular Carcinoma Through PI3K/AKT Signaling.

Chengwu Gong, Jiyuan Ai, Yun Fan, Jun Gao, Weiwei Liu, Qian Feng, Wenjun Liao, Linquan Wu

Open access · goldAbstract read
In one paragraph

Article in OncoTargets and therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed, 1 pooled it
6.9field-weighted citation impact, top 2% of its field
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

73 citing papers in PubMed, 1 synthesis or guideline pooled it, 118 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Hepatocellular carcinoma: signaling pathways and therapeutic advances.Signal transduction and targeted therapy · 2025
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  8. Review
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  12. Article
  13. Article
  14. Role and mechanism ofFrontiers in pharmacology · 2024
    Article
  15. Association ofFrontiers in veterinary science · 2024
    Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article

13 more citing papers are in PubMed but not listed here.

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

8 authors at 3 institutions in 1 country.

Chengwu Gong *Department of General Surgery, The Second Affiliated Hospital of Nanchang University, Nanchang 330006, People's Republic of China.
Jiyuan Ai *Department of General Surgery, The Second Affiliated Hospital of Nanchang University, Nanchang 330006, People's Republic of China.
Yun FanDepartment of Neurology, Tongji Hospital, Huazhong University of Science and Technology, Wuhan 430000, People's Republic of China.
Jun GaoDepartment of General Surgery, The Second Affiliated Hospital of Nanchang University, Nanchang 330006, People's Republic of China.
Weiwei LiuDepartment of General Surgery, The Second Affiliated Hospital of Nanchang University, Nanchang 330006, People's Republic of China.
Qian FengDepartment of Emergency Medicine, The Second Affiliated Hospital of Nanchang University, Nanchang 330006, People's Republic of China.
Wenjun LiaoDepartment of General Surgery, The Second Affiliated Hospital of Nanchang University, Nanchang 330006, People's Republic of China.
Linquan WuDepartment of General Surgery, The Second Affiliated Hospital of Nanchang University, Nanchang 330006, People's Republic of China.
Nanchang University · CNSecond Affiliated Hospital of Nanchang University · CNHuazhong University of Science and Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeStudies show that high expression of non-SMC condensin I complex subunit G (NCAPG) is associated with many tumors. In this study, we explore the mechanism by which NCAPG promotes proliferation in hepatocellular carcinoma (HCC). PATIENTS AND

methodsLiver cancer and paracancerous tissue specimens of 90 HCC patients were collected, and expression levels of NCAPG in these tissues and cell lines were evaluated by Western blotting and immunohistochemistry. HCC cells were transfected with siRNAs and plasmids, and pathway activators or inhibitors were added. The 5-ethynyl-2'-deoxyuridine (EdU) proliferation assay was used to measure cell proliferation. Flow cytometry was used to evaluate cell apoptosis. Western blot assays were performed as a standard procedure to detect total protein expression. Treated HCC cells were subcutaneously injected into nude mice.

resultsAnalysis using the Oncomine database showed that NCAPG was upregulated in HCC and immunohistochemistry and Western blot assays showed it was upregulated in both HCC tissues and HCC cell lines. The overexpression of NCAPG could promote HCC cell proliferation and reduce HCC cell apoptosis. More importantly, RNA-sequencing analysis predicted that NCAPG plays a role in the HCC via PI3K-AKT signaling pathway. The PI3K/AKT/FOXO4 pathway was aberrantly activated, and the expressions of apoptosis-related protein were altered when NCAPG was overexpressed or silenced both in vitro and in vivo. LY294002, a PI3K inhibitor, could eliminate the NCAPG role of promoting HCC cell proliferation and reducing HCC cell apoptosis, while 740Y-P, a PI3K activator, contributed to the opposite effect.

conclusionNCAPG functions as an oncogene in HCC and plays a role in promoting cell proliferation and antiapoptosis through activating the PI3K/AKT/FOXO4 pathway.

Indexed as

FOXO4hepatocellular carcinomaNCAPGPI3K/AKTproliferation

Identifiers

PMID31802891
PMCPMC6801502
OpenAlexW2980812453

What OpenQuestion holds

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LicenceCC BY-NC
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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.