Evidence map›Paper›PMID 35695994›Full record

ArticleMolecular biomedicine2022

The inhibition of protein translation promotes tumor angiogenic switch.

Hui Luo, Yuge Shen, Weiting Liao, Qiqi Li, Ni Wu, Jian Zhong, Chaoxin Xiao, Jia Gan, Yun Yang, E Dong and 8 more

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular biomedicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.4field-weighted citation impact, top 47% 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

1 citing paper in PubMed, 4 citations in OpenAlex.

  1. Article
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

18 authors at 3 institutions in 1 country.

Hui Luo *State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University and Collaborative Innovation Center, No.17 Renmin South Road Section Three, Chengdu, 610041, Sichuan, China.
Yuge Shen *State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University and Collaborative Innovation Center, No.17 Renmin South Road Section Three, Chengdu, 610041, Sichuan, China.
Weiting Liao *State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University and Collaborative Innovation Center, No.17 Renmin South Road Section Three, Chengdu, 610041, Sichuan, China.
Qiqi LiState Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University and Collaborative Innovation Center, No.17 Renmin South Road Section Three, Chengdu, 610041, Sichuan, China.
Ni WuThe Third Affiliated Hospital of Chengdu Medical College,Pidu District People's Hospital, Chengdu, China.
Jian ZhongState Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University and Collaborative Innovation Center, No.17 Renmin South Road Section Three, Chengdu, 610041, Sichuan, China.
Chaoxin XiaoState Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University and Collaborative Innovation Center, No.17 Renmin South Road Section Three, Chengdu, 610041, Sichuan, China.
Jia GanState Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University and Collaborative Innovation Center, No.17 Renmin South Road Section Three, Chengdu, 610041, Sichuan, China.
Yun YangState Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University and Collaborative Innovation Center, No.17 Renmin South Road Section Three, Chengdu, 610041, Sichuan, China.
E DongState Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University and Collaborative Innovation Center, No.17 Renmin South Road Section Three, Chengdu, 610041, Sichuan, China.
Guimin ZhangState Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University and Collaborative Innovation Center, No.17 Renmin South Road Section Three, Chengdu, 610041, Sichuan, China.
Binrui LiuState Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University and Collaborative Innovation Center, No.17 Renmin South Road Section Three, Chengdu, 610041, Sichuan, China.
Xiaozhu YueState Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University and Collaborative Innovation Center, No.17 Renmin South Road Section Three, Chengdu, 610041, Sichuan, China.
Lin XuState Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University and Collaborative Innovation Center, No.17 Renmin South Road Section Three, Chengdu, 610041, Sichuan, China.
Yan LiuState Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University and Collaborative Innovation Center, No.17 Renmin South Road Section Three, Chengdu, 610041, Sichuan, China.
Chengjian ZhaoState Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University and Collaborative Innovation Center, No.17 Renmin South Road Section Three, Chengdu, 610041, Sichuan, China.
Qian ZhongDepartment of Gynecology and Obstetrics, West China Second University Hospital of Sichuan University, Chengdu, China. cdcd91761@163.com.
Hanshuo YangState Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University and Collaborative Innovation Center, No.17 Renmin South Road Section Three, Chengdu, 610041, Sichuan, China. yhansh@scu.edu.cn.
Sichuan University · CNChengdu Third People's Hospital · CNWest China Second University Hospital of Sichuan University · CN

Funding

National Natural Science Foundation of China 81171956National Natural Science Foundation of China 81272216
6 · The paper itself

Abstract

The 'angiogenic switch' is critical for tumor progression. However, the pathological details and molecular mechanisms remain incompletely characterized. In this study, we established mammal xenografts in zebrafish to visually investigate the first vessel growth (angiogenic switch) in real-time, by inoculating tumor cells into the perivitelline space of live optically transparent Transgenic (flk1:EGFP) zebrafish larvae. Using this model, we found that hypoxia and hypoxia-inducible factor (HIF) signaling were unnecessary for the angiogenic switch, whereas vascular endothelial growth factor A gene (Vegfa) played a crucial role. Mechanistically, transcriptome analysis showed that the angiogenic switch was characterized by inhibition of translation, but not hypoxia. Phosphorylation of eukaryotic translation initiation factor 2 alpha (Eif2α) and the expression of Vegfa were increased in the angiogenic switch microtumors, and 3D tumor spheroids, and puromycin-treated tumor cells. Vegfa overexpression promoted early onset of the angiogenic switch, whereas Vegfa knockout prevented the first tumor vessel from sprouting. Pretreatment of tumor cells with puromycin promoted the angiogenic switch in vivo similarly to Vegfa overexpression, whereas Vegfa knockdown suppressed the increase. This study provides direc and dynamic in vivo evidences that inhibition of translation, but not hypoxia or HIF signaling promotes the angiogenic switch in tumor by increasing Vegfa transcription.

Indexed as

Angiogenic switchHIFMicrotumorProtein translationVegfa

Identifiers

PMID35695994
PMCPMC9192909
OpenAlexW4282549772

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.