Evidence map›Paper›PMID 36607591›Full record

ArticleClinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico2023

HNF4G stimulates the development of pancreatic cancer by promoting IGF2BP2 transcription.

Jian Zhan, Qian Zhang, Xu Tong, Xu Liu, Chunbo Zhao

Abstract read
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In one paragraph

Article in Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

5 citing papers in PubMed, 8 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

5 authors at 1 institution in 1 country.

Jian Zhan *Department of Abdominal Radiotherapy, Harbin Medical University Cancer Hospital, Harbin Medical University, 150 Haping Road, Nangang District, Harbin, 150081, Heilongjiang, China.
Qian Zhang *Department of Abdominal Radiotherapy, Harbin Medical University Cancer Hospital, Harbin Medical University, 150 Haping Road, Nangang District, Harbin, 150081, Heilongjiang, China.
Xu TongDepartment of Abdominal Radiotherapy, Harbin Medical University Cancer Hospital, Harbin Medical University, 150 Haping Road, Nangang District, Harbin, 150081, Heilongjiang, China.
Xu LiuDepartment of Abdominal Radiotherapy, Harbin Medical University Cancer Hospital, Harbin Medical University, 150 Haping Road, Nangang District, Harbin, 150081, Heilongjiang, China.
Chunbo ZhaoDepartment of Abdominal Radiotherapy, Harbin Medical University Cancer Hospital, Harbin Medical University, 150 Haping Road, Nangang District, Harbin, 150081, Heilongjiang, China. Zhaochunbo8629@163.com.ORCID http://orcid.org/0000-0002-4769-9424
Harbin Medical University · CN

Funding

Special Fund for Clinical Research of Wu Jieping Medical Foundation NO.320.6750.2020-12-08
6 · The paper itself

Abstract

objectivePancreatic cancer is a devastating and lethal malignancy. Our study investigated the effective mechanism of HNF4G on pancreatic cancer cell functions through the IGF2BP2 transcription.

methodsHNF4G and IGF2BP2 expressions in pancreatic cancer were examined. The relationship between HNF4G expression and pancreatic cancer patients' clinicopathological characteristics was evaluated. After interfering with HNF4G expression in pancreatic cancer cells, the cell proliferative, migratory, and invasive capabilities were evaluated. Also, the expression of proliferation-related gene PCNA and migration and invasion-related gene MMP2 was determined. The binding relation between HNF4G and HNF4G promoter was forecasted and testified. A tumorigenesis assay in nude mice was performed to detect the HNF4G interference's effect on the subcutaneous tumorigenic capacity of pancreatic cancer cells.

resultsHNF4G and IGF2BP2 expressions were up-regulated in pancreatic cancer. Specifically, interfering with HNF4G inhibited PANC-1 cell proliferative, invasive and migratory behaviors, and decreased PCNA and MMP2 expression. Mechanistically, HNF4G as a transcription factor could specifically bind to IGF2BP2 and promote its expression. Rescue assay findings showed that IGF2BP2 overexpression could reverse the inhibiting effect of HNF4G interference on pancreatic cancer cells. For the in vivo finding, interfering HNF4G expression retarded the subcutaneous tumorigenic ability of pancreatic cancer cells.

conclusionWe summarize that HNF4G as a transcription factor regulates IGF2BP2 expression to promote pancreatic cancer cell proliferation and migration capacities.

Indexed as

Pancreatic NeoplasmsAnimalsCell Line, TumorCell MovementCell ProliferationGene Expression Regulation, NeoplasticHepatocyte Nuclear Factor 4HumansMatrix Metalloproteinase 2MiceMice, NudeProliferating Cell Nuclear AntigenRNA-Binding ProteinsTranscription FactorsHepatocyte Nuclear Factor 4Hnf4a protein, mouseHNF4G protein, humanIGF2BP2 protein, humanIGF2BP2 protein, mouseMatrix Metalloproteinase 2MMP2 protein, humanMmp2 protein, mousePCNA protein, humanProliferating Cell Nuclear AntigenRNA-Binding ProteinsTranscription FactorsHNF4GIGF2BP2MigrationPancreatic cancerProliferationTranscription factor

Identifiers

PMID36607591
OpenAlexW4313640144

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.