Evidence map›Paper›PMID 30643426›Full record

ArticleOncoTargets and therapy2019

CD4

Chunying Shi, Ying Chen, Yaodong Chen, Yuchuan Yang, Wang Bing, Jiping Qi

Open access · goldAbstract read
PubMed Full text at PMC Publisher
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 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.5field-weighted citation impact, top 8% 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

36 citing papers in PubMed, 56 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

6 authors at 2 institutions in 1 country.

Chunying ShiDepartment of Radiology, The First Affiliated Hospital of Harbin Medical University, Heilongjiang, Harbin 150001, China.
Ying ChenDepartment of Radiology, The First Affiliated Hospital of Harbin Medical University, Heilongjiang, Harbin 150001, China.
Yaodong ChenDepartment of Radiology, The First Affiliated Hospital of Harbin Medical University, Heilongjiang, Harbin 150001, China.
Yuchuan YangDepartment of Radiology, The First Affiliated Hospital of Harbin Medical University, Heilongjiang, Harbin 150001, China.
Wang BingDepartment of Radiology, The First Affiliated Hospital of Harbin Medical University, Heilongjiang, Harbin 150001, China.
Jiping QiDepartment of Pathology, The First Affiliated Hospital of Harbin Medical University, Heilongjiang, Harbin 150001, China, qjpbingli5487@sina.com.
First Affiliated Hospital of Harbin Medical University · CNHarbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCD4

methodsThe mechanism of Tregs in the invasion and metastasis of HCC was investigated in vivo and in vitro using immunohistochemical analysis, western blot, and quantitative reverse transcription-PCR (qRT-PCR).

resultsAnalysis of 78 clinical HCC samples indicated that high expression of Tregs was strongly associated with poor cancer-free survival and overall survival of patients. The reduced expression of E-cadherin and enhanced expression of Vimentin and transforming growth factor-beta 1 (TGF-β1) were found in HCC tissue compared with normal liver tissue. The HCC Hepa1-6 cells were treated with the supernatant of Tregs-conditioned medium (Tregs-CM) to investigate the epithelial-mesenchymal transition (EMT) and TGF-β1. Western blot and qRT-PCR also showed that down-regulated E-cadherin and up-regulated Vimentin and TGF-β1 were found in Tregs-CM-treated Hepa1-6 cells. An experiment of tumorigenicity in C57 mice showed larger and heavier tumors in Tregs-CM-treated group than in the control group. Tregs produced higher TGF-β1 compared with Tregs treated with FOXP3 shRNA. TGF-β1 with neutralizing antibodies was used to deplete TGF-β1 in Tregs-CM, which enhanced expression of E-cadherin, reduced expression of Vimentin and TGF-β1, and decreased migratory and invasive capacity of Hepa1-6 cells.

conclusionTregs could promote the invasion and migration of Hepa1-6 cells, which are possibly maintained by TGF-β1-induced EMT. This study showed that the development of therapeutic strategies against TGF-β1 pathway is valuable in HCC therapy.

Indexed as

CD4+ CD25+ regulatory T cellsepithelial to mesenchymal transitionhepatocellular carcinomaTGF-β1

Identifiers

PMID30643426
PMCPMC6314313
OpenAlexW2908198004

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.