Evidence map›Paper›PMID 37162505›Full record

ArticleThe Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology2023

Fibulin-2 Facilitates Malignant Progression of Hepatocellular Carcinoma.

Xinyan Hu, Tianze Liu, Luting Li, Hairun Gan, Tiancheng Wang, Pengfei Pang, Junjie Mao

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.9field-weighted citation impact, top 21% 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

3 citing papers in PubMed, 3 citations in OpenAlex.

  1. Review
  2. Article
  3. Lung Inflammatory Phenotype in Mice Deficient in Fibulin-2 and ADAMTS-12.International journal of molecular sciences · 2024
    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

7 authors at 1 institution in 1 country.

Xinyan HuDepartment of Interventional Medicine, The Fifth Affiliated Hospital, Sun Yat-sen University, Zhuhai, China ; Guangdong Provincial Key Laboratory of Biomedical Imaging, The Fifth Affiliated Hospital, Sun Yat-sen University, Zhuhai, China;Guangdong Provincial Engineering Research Center of Molecular Imaging, The Fifth Affiliated Hospital, Sun Yat-sen University, Zhuhai, China;Institute of Interventional Radiology, Sun Yat-sen University, Zhuhai, China.
Tianze LiuThe Cancer Center, The Fifth Affiliated Hospital, Sun Yat-sen University, Zhuhai, Guangdong Province, China.
Luting LiDepartment of Interventional Medicine, The Fifth Affiliated Hospital, Sun Yat-sen University, Zhuhai, China ; Guangdong Provincial Key Laboratory of Biomedical Imaging, The Fifth Affiliated Hospital, Sun Yat-sen University, Zhuhai, China;Guangdong Provincial Engineering Research Center of Molecular Imaging, The Fifth Affiliated Hospital, Sun Yat-sen University, Zhuhai, China;Institute of Interventional Radiology, Sun Yat-sen University, Zhuhai, China.
Hairun GanDepartment of Interventional Medicine, The Fifth Affiliated Hospital, Sun Yat-sen University, Zhuhai, China ; Guangdong Provincial Key Laboratory of Biomedical Imaging, The Fifth Affiliated Hospital, Sun Yat-sen University, Zhuhai, China;Guangdong Provincial Engineering Research Center of Molecular Imaging, The Fifth Affiliated Hospital, Sun Yat-sen University, Zhuhai, China;Institute of Interventional Radiology, Sun Yat-sen University, Zhuhai, China.
Tiancheng WangDepartment of Interventional Medicine, The Fifth Affiliated Hospital, Sun Yat-sen University, Zhuhai, China ; Guangdong Provincial Key Laboratory of Biomedical Imaging, The Fifth Affiliated Hospital, Sun Yat-sen University, Zhuhai, China;Guangdong Provincial Engineering Research Center of Molecular Imaging, The Fifth Affiliated Hospital, Sun Yat-sen University, Zhuhai, China;Institute of Interventional Radiology, Sun Yat-sen University, Zhuhai, China.
Pengfei PangDepartment of Interventional Medicine, The Fifth Affiliated Hospital, Sun Yat-sen University, Zhuhai, China; Guangdong Provincial Engineering Research Center of Molecular Imaging, The Fifth Affiliated Hospital, Sun Yat-sen University, Zhuhai, China;Institute of Interventional Radiology, Sun Yat-sen University, Zhuhai, China.
Junjie MaoDepartment of Interventional Medicine, The Fifth Affiliated Hospital, Sun Yat-sen University, Zhuhai, China; Guangdong Provincial Engineering Research Center of Molecular Imaging, The Fifth Affiliated Hospital, Sun Yat-sen University, Zhuhai, China;Institute of Interventional Radiology, Sun Yat-sen University, Zhuhai, China.
Sun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIdentification of biomarkers to assist in the clinical management of hepatocellular carcinoma represents an urgent requirement. Fibulin-2 is known to contribute to the development and progression of various cancer types. This research investigated the role of fibulin-2 in hepatocellular carcinoma and explored the possible mechanisms.

methodsThe expression of fibulin-2 in hepatocellular carcinoma was measured by bioinformatic analysis and confirmed by western blot and immunohistochemical staining in cell lines or patients' samples. The clinicopathologic features of hepatocellular carcinoma patients was analyzed. Cell viability assays were used to explore the role of fibulin-2 on proliferation in hepatocellular carcinoma. Western blot was conducted to uncover changes of protein expression of Ras-MEK-ERK1/2 pathway when Fibulin-2 was overexpressed or silenced. Flow cytometry analyses were used to determine the roles of fibulin-2 in the function of apoptosis and cell cycle. Subcutaneous xenograft mouse models showed the tumor growth pattern after fibulin-2 silence in vivo.

resultsWe reported the upregulation of fibulin-2 in most hepatocellular carcinoma tissues and cells lines. Fibulin-2 promoted the proliferation of hepatocellular carcinoma cells in vitro by regulating Ras-MEK-ERK1/2 signaling pathway, whereas knockdown of fibulin-2 incurred the opposite effect on proliferation. Consistently, knockdown of fibulin-2 resulted in increased apoptosis and induced growth arrest during the G0/G1 phase transition. In vivo xenograft assessment confirmed that knockdown of fibulin-2 inhibited hepatocellular carcinoma tumor growth.

conclusionsFibulin-2 exhibited tumor promotor activities in malignant progression of hepatocellular carcinoma. The results of the study highlighted the potential of fibulin-2 to be utilized as a promising biomarker and therapeutic target for hepatocellular carcinoma.

Indexed as

Carcinoma, HepatocellularLiver NeoplasmsAnimalsApoptosisCalcium-Binding ProteinsCell ProliferationExtracellular Matrix ProteinsGene Expression Regulation, NeoplasticHumansMiceMitogen-Activated Protein Kinase KinasesCalcium-Binding ProteinsExtracellular Matrix Proteinsfibulin 2Mitogen-Activated Protein Kinase Kinases

Identifiers

PMID37162505
PMCPMC10441129
OpenAlexW4376113771

What OpenQuestion holds

Textmetadata
LicenceCC BY
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 OpenQuestion graph.