Evidence map›Paper›PMID 33004943›Full record

ArticleScientific reports2020

VEGF knockdown enhances radiosensitivity of nasopharyngeal carcinoma by inhibiting autophagy through the activation of mTOR pathway.

Li Chen, Guoxiang Lin, Kaihua Chen, Fangzhu Wan, Renba Liang, Yongchu Sun, Xishan Chen, Xiaodong Zhu

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.6field-weighted citation impact, top 9% 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

20 citing papers in PubMed, 31 citations in OpenAlex.

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  18. A functional outside-in signaling network of proteoglycans and matrix molecules regulating autophagy.Matrix biology : journal of the International Society for Matrix Biology · 2021
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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 1 institution in 1 country.

Li Chen *Department of Radiation Oncology, Guangxi Medical University Cancer Hospital, Nanning, 530021, Guangxi, People's Republic of China.
Guoxiang Lin *Department of Oncology, Wuming Hospital of Guangxi Medical University, Nanning, 530010, Guangxi, People's Republic of China.
Kaihua ChenDepartment of Radiation Oncology, Guangxi Medical University Cancer Hospital, Nanning, 530021, Guangxi, People's Republic of China.
Fangzhu WanDepartment of Radiation Oncology, Guangxi Medical University Cancer Hospital, Nanning, 530021, Guangxi, People's Republic of China.
Renba LiangDepartment of Radiation Oncology, Guangxi Medical University Cancer Hospital, Nanning, 530021, Guangxi, People's Republic of China.
Yongchu SunDepartment of Radiation Oncology, Guangxi Medical University Cancer Hospital, Nanning, 530021, Guangxi, People's Republic of China.
Xishan ChenDepartment of Radiation Oncology, Guangxi Medical University Cancer Hospital, Nanning, 530021, Guangxi, People's Republic of China.
Xiaodong ZhuDepartment of Radiation Oncology, Guangxi Medical University Cancer Hospital, Nanning, 530021, Guangxi, People's Republic of China. zhuxdonggxmu@126.com.
Guangxi Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Vascular endothelial growth factor (VEGF) is an important pro-angiogenic factor. VEGF was reported to promote the occurrence of autophagy, which enhanced the radioresistance of tumors. The purpose of this study was to investigate the influence of VEGF silencing on the radiosensitivity of nasopharyngeal carcinoma (NPC) cells and the underlying mechanisms. The radiosensitivity of NPC cells after VEGF silencing was detected by cell counting kit 8 (CCK-8) and clonogenic assay, while cell cycle and apoptosis were detected by flow cytometry. The processes of DNA damage, repair and autophagy were examined by immunofluorescence and western blotting. The interaction between VEGF and mTOR was confirmed by western blotting and co-immunoprecipitation studies. The effect of VEGF on radiosensitivity of NPC cells was investigated in vivo using a xenograft model. Furthermore, immunohistochemistry and TUNEL assays were used to verify the relationship between autophagy and radiosensitivity in NPC after VEGF depletion. Downregulation of VEGF significantly inhibited cell proliferation and induced apoptosis of NPC cells after radiotherapy in vitro and in vivo. In addition, VEGF knockdown not only decreased autophagy level, but also delayed the DNA damage repair in NPC cells after irradiation. Mechanistically, silencing VEGF suppressed autophagy through activation of the mTOR pathway. VEGF depletion increased radiosensitivity of NPC cells by suppressing autophagy via activation of the mTOR pathway.

Indexed as

AutophagyAnimalsCell Line, TumorGene Knockdown TechniquesHumansMaleMiceMice, Inbred BALB CMice, NudeNasopharyngeal CarcinomaNasopharyngeal NeoplasmsNeoplasm TransplantationRadiation ToleranceTOR Serine-Threonine KinasesVascular Endothelial Growth Factor AMTOR protein, humanTOR Serine-Threonine KinasesVascular Endothelial Growth Factor AVEGFA protein, human

Identifiers

PMID33004943
PMCPMC7531011
OpenAlexW3090213895

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.