Evidence map›Paper›PMID 30662352›Full record

ArticleInternational journal of biological sciences2019

COPI-Mediated Nuclear Translocation of EGFRvIII Promotes STAT3 Phosphorylation and PKM2 Nuclear Localization.

Mingzhi Zhang, Haojie Sun, Yue Deng, Ming Su, Shiruo Wei, Peipei Wang, Lanlan Yu, Jinwen Liu, Jinhai Guo, Xuan Wang and 3 more

Open access · goldAbstract read
In one paragraph

Article in International journal of biological sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
0.5field-weighted citation impact, top 36% 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, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.

  1. Pooled it
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  13. Frontiers in oncology · 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

13 authors at 1 institution in 1 country.

Mingzhi ZhangDepartment of Cell Biology, Stem Cell Research Center, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, People's Republic of China.
Haojie SunNeuroscience Research Institute, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, People's Republic of China.
Yue DengBeijing Cellonis Biotechnologies Co. Ltd, Zhongguancun Bio-Medicine Park, Beijing, People's Republic of China.
Ming SuDepartment of Cell Biology, Stem Cell Research Center, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, People's Republic of China.
Shiruo WeiDepartment of Cell Biology, Stem Cell Research Center, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, People's Republic of China.
Peipei WangBeijing Cellonis Biotechnologies Co. Ltd, Zhongguancun Bio-Medicine Park, Beijing, People's Republic of China.
Lanlan YuBeijing DongFang YaMei Gene Science and Technology Research Institute, Beijing, People's Republic of China.
Jinwen LiuBeijing DongFang YaMei Gene Science and Technology Research Institute, Beijing, People's Republic of China.
Jinhai GuoBeijing DongFang YaMei Gene Science and Technology Research Institute, Beijing, People's Republic of China.
Xuan WangResearch Center of Artificial Organ and Tissue Engineering, Second Department of Hepatobiliary Surgery, ZhuJiang Hospital, Southern Medical University, Guangzhou, Guangdong Province, People's Republic of China.
Xu HanResearch Center of Artificial Organ and Tissue Engineering, Second Department of Hepatobiliary Surgery, ZhuJiang Hospital, Southern Medical University, Guangzhou, Guangdong Province, People's Republic of China.
Qihua HeMedical and Health Analytical Center, Peking University Health Science Center, People's Republic of China.
Li ShenDepartment of Cell Biology, Stem Cell Research Center, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, People's Republic of China.
Peking University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

As a non-ligand-dependent activation protein, EGFRvIII is the most common mutant of EGFR, and its existence or especially its nuclear translocation in tumors can exacerbate the malignancy. Compared with the nuclear translocation of EGFR, which has been studied extensively, the specific mechanism by which EGFRvIII undergoes nuclear translocation has not yet been reported. Here, we found that EGFRvIII eventually reached the nucleus with the involvement of the Golgi and endoplasmic reticulum (ER) in glioma cells. In this process, syntaxin-6 was responsible for the identification and transport of EGFRvIII on Golgi. We also demonstrated that COPI mediated the reverse transport of EGFRvIII from the Golgi to ER, which process was also important for EGFRvIII's nuclear accumulation. EGFRvIII's nuclear translocation can significantly promote STAT3 phosphorylation and PKM2 nuclear localization. Finally, we showed that EGFRvIII's nuclear translocation obviously induced the growth of gliomas in an intracranial xenotransplantation experiment. These data suggested that searching methods that inhibit EGFRvIII entry into the nucleus will be effective glioma treatments.

Indexed as

AnimalsCell LineCell NucleusEndoplasmic ReticulumErbB ReceptorsFemaleFluorescent Antibody TechniqueGlioblastomaGliomaHumansImmunoblottingImmunohistochemistryImmunoprecipitationMiceMice, Inbred BALB CMice, Nudeepidermal growth factor receptor VIIIErbB ReceptorsSTAT3 Transcription FactorCOPIEGFRvIIInuclear translocationPKM2 nuclear localizationSyntaxin-6

Identifiers

PMID30662352
PMCPMC6329918
OpenAlexW2904064222

What OpenQuestion holds

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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.