Evidence map›Paper›PMID 28565871›Full record

ArticleExperimental and therapeutic medicine2017

Propofol inhibits hepatocellular carcinoma growth and invasion through the HMGA2-mediated Wnt/β-catenin pathway.

Wei Ou, Jie Lv, Xiaohua Zou, Yin Yao, Jinli Wu, Jian Yang, Zhumei Wang, Yan Ma

Open access · diamondAbstract read
In one paragraph

Article in Experimental and therapeutic medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
4.2field-weighted citation impact, top 5% 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

25 citing papers in PubMed, 46 citations in OpenAlex.

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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

8 authors at 2 institutions in 1 country.

Wei OuDepartment of Anesthesiology, The Affiliated Hospital of Guizhou Medical University, Guizhou, Guiyang 550001, P.R. China.
Jie LvDepartment of Anesthesiology, The Affiliated Hospital of Guizhou Medical University, Guizhou, Guiyang 550001, P.R. China.
Xiaohua ZouDepartment of Anesthesiology, The Affiliated Hospital of Guizhou Medical University, Guizhou, Guiyang 550001, P.R. China.
Yin YaoDepartment of Anesthesiology, The Affiliated Hospital of Guizhou Medical University, Guizhou, Guiyang 550001, P.R. China.
Jinli WuDepartment of Anesthesiology, The Affiliated Hospital of Guizhou Medical University, Guizhou, Guiyang 550001, P.R. China.
Jian YangDepartment of Anesthesiology, The Affiliated Hospital of Guizhou Medical University, Guizhou, Guiyang 550001, P.R. China.
Zhumei WangDepartment of Anesthesiology, The Affiliated Hospital of Guizhou Medical University, Guizhou, Guiyang 550001, P.R. China.
Yan MaDepartment of Anesthesiology, The Affiliated Hospital of Guizhou Medical University, Guizhou, Guiyang 550001, P.R. China.
Affiliated Hospital of Guizhou Medical University · CNGuiyang Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Propofol is a commonly used intravenous anesthetic in tumor surgery. Recently, studies have confirmed that propofol has an antitumor effect on hepatocellular carcinoma (HCC); however, the molecular mechanism underlying this effect has not been elucidated until now. The present study aimed to investigate the mechanism of propofol on HepG2 cell proliferation, apoptosis and invasion, focusing on High Mobility Group AT-Hook 2 (HMGA2)-mediated Wnt/β-catenin pathway. The HepG2 cells were treated with various concentrations of propofol for 24 h, the relative protein levels of HMGA2, Wnt3a, β-catenin, Snail Family Zinc Finger 1 and c-myc were determined by western blot analysis. HMGA2-pcDNA3.1 plasmid was transfected into the HepG2 cells to overexpress HMGA2. Cell proliferation, apoptosis and invasion were examined by MTT assays, flow cytometry and Transwell-matrigel invasion assays, respectively. The results showed that propofol suppressed HMGA2 expression and Wnt/β-catenin signaling in a dose-dependent manner. Propofol was able to inhibit cell proliferation and invasion, and induce cell apoptosis of HepG2 cells; however, these effects were attenuated by HMGA2 overexpression. The suppressed Wnt/β-catenin signaling in HepG2 cells by treatment with propofol was also reversed by HMGA2 overexpression. In conclusion, this study provided a novel mechanism underlying the anti-tumor function of propofol on HCC. To the best of our knowledge, the present study is the first to demonstrate that propofol could downregulate the expression of HMGA2, which inhibited the Wnt/β-catenin pathway, thus leading to the inhibition of cell proliferation and invasion, as well as the apoptosis of HepG2 cells.

Indexed as

hepatocellular carcinomaHigh Mobility Group AT-Hook 2propofolWnt/β-catenin

Identifiers

PMID28565871
PMCPMC5443290
OpenAlexW2600570188

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.