Evidence map›Paper›PMID 32064160›Full record

ArticleAmerican journal of cancer research2020

EIF3H interacts with PDCD4 enhancing lung adenocarcinoma cell metastasis.

Yingying Hu, Xiao Wei, Yumin Lv, Xin Xie, Liu Yang, Jingjing He, Xingyu Tao, Yuting Ma, Yun Su, Liyang Wu and 2 more

Open access · greenAbstract read
In one paragraph

Article in American journal of cancer research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.0field-weighted citation impact, top 28% 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

16 citing papers in PubMed, 22 citations in OpenAlex.

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  8. The therapeutic potential of RNA m(6)A in lung cancer.Cell communication and signaling : CCS · 2024
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    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

12 authors at 2 institutions in 1 country.

Yingying HuAffiliated Cancer Hospital & Institute of Guangzhou Medical University, Guangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Degradation, State Key Laboratory of Respiratory Disease, School of Basic Medical Sciences, Guangzhou Medical University Guangzhou 510095, Guangdong, P. R. China.
Xiao WeiAffiliated Cancer Hospital & Institute of Guangzhou Medical University, Guangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Degradation, State Key Laboratory of Respiratory Disease, School of Basic Medical Sciences, Guangzhou Medical University Guangzhou 510095, Guangdong, P. R. China.
Yumin LvAffiliated Cancer Hospital & Institute of Guangzhou Medical University, Guangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Degradation, State Key Laboratory of Respiratory Disease, School of Basic Medical Sciences, Guangzhou Medical University Guangzhou 510095, Guangdong, P. R. China.
Xin XieAffiliated Cancer Hospital & Institute of Guangzhou Medical University, Guangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Degradation, State Key Laboratory of Respiratory Disease, School of Basic Medical Sciences, Guangzhou Medical University Guangzhou 510095, Guangdong, P. R. China.
Liu YangAffiliated Cancer Hospital & Institute of Guangzhou Medical University, Guangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Degradation, State Key Laboratory of Respiratory Disease, School of Basic Medical Sciences, Guangzhou Medical University Guangzhou 510095, Guangdong, P. R. China.
Jingjing HeAffiliated Cancer Hospital & Institute of Guangzhou Medical University, Guangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Degradation, State Key Laboratory of Respiratory Disease, School of Basic Medical Sciences, Guangzhou Medical University Guangzhou 510095, Guangdong, P. R. China.
Xingyu TaoAffiliated Cancer Hospital & Institute of Guangzhou Medical University, Guangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Degradation, State Key Laboratory of Respiratory Disease, School of Basic Medical Sciences, Guangzhou Medical University Guangzhou 510095, Guangdong, P. R. China.
Yuting MaAffiliated Cancer Hospital & Institute of Guangzhou Medical University, Guangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Degradation, State Key Laboratory of Respiratory Disease, School of Basic Medical Sciences, Guangzhou Medical University Guangzhou 510095, Guangdong, P. R. China.
Yun SuAffiliated Cancer Hospital & Institute of Guangzhou Medical University, Guangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Degradation, State Key Laboratory of Respiratory Disease, School of Basic Medical Sciences, Guangzhou Medical University Guangzhou 510095, Guangdong, P. R. China.
Liyang WuAffiliated Cancer Hospital & Institute of Guangzhou Medical University, Guangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Degradation, State Key Laboratory of Respiratory Disease, School of Basic Medical Sciences, Guangzhou Medical University Guangzhou 510095, Guangdong, P. R. China.
Weiyi FangCancer Institute, Southern Medical University Guangzhou 510515, Guangdong, P. R. China.
Zhen LiuAffiliated Cancer Hospital & Institute of Guangzhou Medical University, Guangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Degradation, State Key Laboratory of Respiratory Disease, School of Basic Medical Sciences, Guangzhou Medical University Guangzhou 510095, Guangdong, P. R. China.
Guangzhou Medical University · CNSouthern Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lung adenocarcinoma (LUAD) is a common type of lung cancer characterized by a high incidence of local invasion and metastasis. Programmed cell death factor 4 (PDCD4) is a well-recognized tumor suppressor gene involved in LUAD, however its precise regulatory mechanism remains elusive. This is the first study to report an inverse regulatory relationship between PDCD4 and eukaryotic translation initiation factor 3 subunit H (EIF3H) in LUAD. Co-immunoprecipitation assays combined with mass spectrometry and immunofluorescent co-localization indicated that PDCD4 interacted with EIF3H. Overexpression of PDCD4 in LUAD cells reduced EIF3H mRNA and protein levels by suppressing c-Jun-induced EIF3H transcription. Further, an elevated level of EIF3H protein was found in LUAD tissues compared with para-cancerous normal lung tissues, and was found to be an unfavorable factor promoting LUAD pathogenesis. Moreover, the negative correlation between PDCD4 and EIF3H protein expression was confirmed in LUAD tissues. Functional analyses showed that EIF3H overexpression promoted LUAD cell migration and invasion

Indexed as

EIF3HinvasionLung adenocarcinomametastasisPDCD4

Identifiers

PMID32064160
PMCPMC7017739
OpenAlexW3009228336

What Socratic holds

Textmetadata
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 Socratic graph.