Evidence map›Paper›PMID 26459253›Full record

ArticleClinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico2016

VEGFR2 inhibition by RNA interference affects cell proliferation, migration, invasion, and response to radiation in Calu-1 cells.

Y Liu, Y Qiao, C Hu, L Liu, L Zhou, B Liu, H Chen, X Jiang

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, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.6field-weighted citation impact, top 32% 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

8 citing papers in PubMed, 14 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.

Y LiuXuzhou Medical College Graduate Academy, Xuzhou, 221006, China.
Y QiaoDepartment of Radiation Oncology, Lianyungang First People's Hospital, No.182, Tongguan Road, Lianyungang City, 222002, Jiangsu Province, China.
C HuDepartment of Radiation Oncology, Lianyungang First People's Hospital, No.182, Tongguan Road, Lianyungang City, 222002, Jiangsu Province, China.
L LiuXuzhou Medical College Graduate Academy, Xuzhou, 221006, China.
L ZhouDepartment of Radiation Oncology, Lianyungang First People's Hospital, No.182, Tongguan Road, Lianyungang City, 222002, Jiangsu Province, China.
B LiuXuzhou Medical College Graduate Academy, Xuzhou, 221006, China.
H ChenXuzhou Medical College Graduate Academy, Xuzhou, 221006, China.
X JiangDepartment of Radiation Oncology, Lianyungang First People's Hospital, No.182, Tongguan Road, Lianyungang City, 222002, Jiangsu Province, China. jxdysy@sohu.com.
The First People’s Hospital of Lianyungang · CNXuzhou Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveTo investigate the role of the vascular endothelial growth factor receptor 2 (VEGFR2) in the proliferation, migration, invasion, and radiation-induced apoptosis of the non-small cell lung cancer (NSCLC) cell line Calu-1.

methodsVEGFR2 gene was silenced by RNA interference in Calu-1 cells, and the expression of VEGFR2 was measured by qRT-PCR and Western blot analysis. The cells were divided into control, VEGF-treated, VEGFR2 knockdown, and VEGFR2 knockdown and VEGF-treated groups. A CCK8 assay and Transwell assay were performed to assess cell proliferation, migration, and invasion, respectively, after VEGFR2 knockdown. Western blot assays were used to detect signaling proteins downstream of VEGFR2. Cells in the groups listed above were also subjected to radiation treatment, followed by apoptosis analysis.

results(1) RNA interference of VEGFR2 in Calu-1 cells reduced VEGFR2 mRNA (P < 0.01) and protein levels (P < 0.01). (2) VEGFR2 knockdown inhibited proliferation (P < 0.05), migration (P < 0.05), and invasion (P < 0.05) in Calu-1 cells. (3) VEGFR2 knockdown blocked the phosphorylation of protein kinase B (Akt, also known as PKB), extracellular regulated kinase (ERK) 1/2, and p38 mitogen-activated protein kinase (p38 MAPK) to various extent (P < 0.05), but did not change their total protein expression. (4) Knockdown of VEGFR2 suppressed HIF-1α protein synthesis (P < 0.05), and exacerbated apoptosis induced by radiation (P < 0.05).

conclusionVEGFR2 gene knockdown significantly suppressed a number of cellular activities in Calu-1 cells and increased radiation-induced cell death.

Indexed as

Cell MovementApoptosisBlotting, WesternCarcinoma, Squamous CellCell Line, TumorCell ProliferationFlow CytometryGene Knockdown TechniquesHumansLung NeoplasmsNeoplasm InvasivenessRadiation ToleranceReal-Time Polymerase Chain ReactionRNA, Small InterferingTransfectionVascular Endothelial Growth Factor Receptor-2KDR protein, humanRNA, Small InterferingVascular Endothelial Growth Factor Receptor-2MigrationProliferationRadiationRNA interferenceVEGFR2

Identifiers

PMID26459253
OpenAlexW1910905929

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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.