Evidence map›Paper›PMID 34373753›Full record

ArticleTheranostics2021

Targeting ATF4-dependent pro-survival autophagy to synergize glutaminolysis inhibition.

Shuting Han, Liyuan Zhu, Yiran Zhu, Yuan Meng, Jiaqiu Li, Ping Song, Neelum Aziz Yousafzai, Lifeng Feng, Miaoqin Chen, Yanmei Wang and 2 more

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

Article in Theranostics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
8.7field-weighted citation impact, top 1% 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

62 citing papers in PubMed, 82 citations in OpenAlex.

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  19. Abnormal changes in metabolites caused by mJournal of advanced research · 2025
    Review
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2 more citing papers are in PubMed but not listed here.

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

12 authors at 4 institutions in 1 country.

Shuting HanDepartment of Medical Oncology, Sir Run Run Shaw Hospital, Medical School of Zhejiang University, Hangzhou, China.
Liyuan ZhuLaboratory of Cancer Biology, Key Lab of Biotherapy, Cancer Center of Zhejiang University, Sir Run Run Shaw Hospital, Medical School of Zhejiang University, Hangzhou, China.
Yiran ZhuLaboratory of Cancer Biology, Key Lab of Biotherapy, Cancer Center of Zhejiang University, Sir Run Run Shaw Hospital, Medical School of Zhejiang University, Hangzhou, China.
Yuan MengLaboratory of Cancer Biology, Key Lab of Biotherapy, Cancer Center of Zhejiang University, Sir Run Run Shaw Hospital, Medical School of Zhejiang University, Hangzhou, China.
Jiaqiu LiDepartment of Medical Oncology, Sir Run Run Shaw Hospital, Medical School of Zhejiang University, Hangzhou, China.
Ping SongDepartment of Medical Oncology, Sir Run Run Shaw Hospital, Medical School of Zhejiang University, Hangzhou, China.
Neelum Aziz YousafzaiDepartment of Allied Health Sciences, University of Poonch Rawalakot, AJK, Pakistan.
Lifeng FengLaboratory of Cancer Biology, Key Lab of Biotherapy, Cancer Center of Zhejiang University, Sir Run Run Shaw Hospital, Medical School of Zhejiang University, Hangzhou, China.
Miaoqin ChenLaboratory of Cancer Biology, Key Lab of Biotherapy, Cancer Center of Zhejiang University, Sir Run Run Shaw Hospital, Medical School of Zhejiang University, Hangzhou, China.
Yanmei WangDepartment of Medical Oncology, Sir Run Run Shaw Hospital, Medical School of Zhejiang University, Hangzhou, China.
Hongchuan JinLaboratory of Cancer Biology, Key Lab of Biotherapy, Cancer Center of Zhejiang University, Sir Run Run Shaw Hospital, Medical School of Zhejiang University, Hangzhou, China.
Xian WangDepartment of Medical Oncology, Sir Run Run Shaw Hospital, Medical School of Zhejiang University, Hangzhou, China.
Sir Run Run Shaw Hospital · CNZhejiang University · CNHangzhou Cancer Hospital · CNUniversity of Poonch Rawalakot

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

As glutamine plays a central role in cancer metabolism, inhibition of glutaminolysis has become an ideal anticancer therapeutic target. However, glutaminolysis inhibition leads to activation of autophagy, which compromises its antitumor effect. Hence, we investigated the mechanism underlying glutaminolysis inhibition-induced pro-survival autophagy.

Indexed as

Activating Transcription Factor 4AnimalsAutophagyCell Line, TumorColorectal NeoplasmsGlutamineHCT116 CellsHumansMaleMiceMice, Inbred C57BLRNA-Binding ProteinsRNA, MessengerRNA StabilityTOR Serine-Threonine KinasesTranscription FactorsActivating Transcription Factor 4ATF4 protein, humanDDIT4 protein, humanGlutamineMTOR protein, humanRNA-Binding ProteinsRNA, MessengerTOR Serine-Threonine KinasesTranscription FactorsATF4DDIT4Glutaminolysis inhibitionmetabolic synthetic lethalityN6-methyladenosine

Identifiers

PMID34373753
PMCPMC8343999
OpenAlexW3184013170

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.