Evidence map›Paper›PMID 33640883›Full record

ArticleAging2021

Maf1 suppression of ATF5-dependent mitochondrial unfolded protein response contributes to rapamycin-induced radio-sensitivity in lung cancer cell line A549.

Chen Lai, Jing Zhang, Zhaohua Tan, Liang F Shen, Rong R Zhou, Ying Y Zhang

Open access · greenAbstract read
In one paragraph

Article in Aging, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 20% 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

14 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 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

6 authors at 2 institutions in 1 country.

Chen LaiDepartment of General Surgery, Xiangya Hospital of Central South University, Changsha 410008, Hunan, China.
Jing ZhangDepartment of Oncology, Xiangya Hospital of Central South University, Changsha 410008, Hunan, China.
Zhaohua TanDepartment of Oncology, Xiangya Hospital of Central South University, Changsha 410008, Hunan, China.
Liang F ShenDepartment of Oncology, Xiangya Hospital of Central South University, Changsha 410008, Hunan, China.
Rong R ZhouDepartment of Oncology, Xiangya Hospital of Central South University, Changsha 410008, Hunan, China.
Ying Y ZhangDepartment of Oncology, Xiangya Hospital of Central South University, Changsha 410008, Hunan, China.
Central South University · CNXiangya Hospital Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

mTOR is well known to promote tumor growth but its roles in enhancing chemotherapy and radiotherapy have not been well studied. mTOR inhibition by rapamycin can sensitize cancer cells to radiotherapy. Here we show that Maf1 is required for rapamycin to increase radio-sensitivity in A549 lung cancer cells. In response to ionizing radiation (IR), Maf1 is inhibited by Akt-dependent re-phosphorylation, which activates mitochondrial unfolded protein response (UPR

Indexed as

A549 CellsActivating Transcription FactorsBlotting, WesternFlow CytometryHumansLung NeoplasmsMitochondriaPhosphorylationRadiation-Sensitizing AgentsRadiation ToleranceReal-Time Polymerase Chain ReactionRepressor ProteinsSirolimusUnfolded Protein ResponseActivating Transcription FactorsATF5 protein, humanMAF1 protein, humanRadiation-Sensitizing AgentsRepressor ProteinsSirolimusMaf1mitochondrial unfolded protein responsemTORnon-small cell lung cancer cellradio-resistance

Identifiers

PMID33640883
PMCPMC7993702
OpenAlexW3133860515

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.