Evidence map›Paper›PMID 29048623›Full record

ArticleOncology reports2017

VEGFR3 inhibition chemosensitizes lung adenocarcinoma A549 cells in the tumor-associated macrophage microenvironment through upregulation of p53 and PTEN.

Ya Li, Yaguang Weng, Liang Zhong, Huimin Chong, Sicheng Chen, Yanting Sun, Wang Li, Qiong Shi

Open access · hybridAbstract read
In one paragraph

Article in Oncology reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.6field-weighted citation impact, top 33% 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

13 citing papers in PubMed, 16 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.

Ya LiDepartment of Laboratory Medicine, M.O.E., Key Laboratory of Laboratory Medicine Diagnostics, Chongqing Medical University, Chongqing 400016, P.R.China.
Yaguang WengDepartment of Laboratory Medicine, M.O.E., Key Laboratory of Laboratory Medicine Diagnostics, Chongqing Medical University, Chongqing 400016, P.R.China.
Liang ZhongDepartment of Laboratory Medicine, M.O.E., Key Laboratory of Laboratory Medicine Diagnostics, Chongqing Medical University, Chongqing 400016, P.R.China.
Huimin ChongDepartment of Laboratory Medicine, M.O.E., Key Laboratory of Laboratory Medicine Diagnostics, Chongqing Medical University, Chongqing 400016, P.R.China.
Sicheng ChenDepartment of Clinical Medicine, Xinxiang Medical University, Xinxiang, Henan 453003, P.R. China.
Yanting SunDepartment of Laboratory Medicine, M.O.E., Key Laboratory of Laboratory Medicine Diagnostics, Chongqing Medical University, Chongqing 400016, P.R.China.
Wang LiDepartment of Laboratory Medicine, M.O.E., Key Laboratory of Laboratory Medicine Diagnostics, Chongqing Medical University, Chongqing 400016, P.R.China.
Qiong ShiDepartment of Laboratory Medicine, M.O.E., Key Laboratory of Laboratory Medicine Diagnostics, Chongqing Medical University, Chongqing 400016, P.R.China.
Chongqing Medical University · CNXinxiang Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In lung adenocarcinoma, loss of p53 and PTEN in tumors are associated with decreased response to chemotherapy and decreased survival. A means to pharmacologically upregulate p53 and PTEN protein expression could improve the prognosis of patients with p53- and PTEN-deficient tumors. In the present study we revealed that vascular endothelial growth factor receptor 3 (VEGFR3) inhibition in lung adenocarcinoma cells was associated with improved expression levels of both p53 and PTEN in the tumor-associated macrophage (TAM) microenvironment. Inhibition of VEGFR3 in lung adenocarcinoma cells was associated with growth arrest and decreased migration and invasion. The upregulation of p53 and PTEN protein expression after VEGFR3 inhibition decreased chemotherapy resistance and improved chemosensitivity in co-cultured A549 cells in which p53 and PTEN expression were decreased. Finally, we demonstrated that TAMs promoted the expression of VEGF-C and its receptor VEGFR3. Western blot analysis revealed the co-cultured A549 cells with TAMs are a primary source of VEGF-C and VEGFR3 in the tumor microenvironment. Our studies revealed that VEGFR3 inhibition may be a pharmacological means to upregulate p53 and PTEN protein expression and improve the outcome of patients with p53- and PTEN-deficient tumors.

Indexed as

Up-RegulationA549 CellsAdenocarcinomaAdenocarcinoma of LungCell MovementCell ProliferationDoxorubicinDrug Resistance, NeoplasmDrug SynergismGene Expression Regulation, NeoplasticHumansIndolesLung NeoplasmsMacrophagesNaphthalenesPTEN Phosphohydrolase3-(4-dimethylamino-naphthalen-1-ylmethylene)-1,3-dihydro-indol-2-oneDoxorubicinFLT4 protein, humanIndolesNaphthalenesPTEN PhosphohydrolasePTEN protein, humanTP53 protein, humanTumor Suppressor Protein p53Vascular Endothelial Growth Factor CVascular Endothelial Growth Factor Receptor-3VEGFC protein, human

Identifiers

PMID29048623
PMCPMC5780029
OpenAlexW2755298694

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.