Evidence map›Paper›PMID 32728173›Full record

ArticleOncogene2020

Impaired AKT signaling and lung tumorigenesis by PIERCE1 ablation in KRAS-mutant non-small cell lung cancer.

Jae-Il Roh, Jaehoon Lee, Young-Hoon Sung, Jahyun Oh, Do Young Hyeon, Yujin Kim, Seungeon Lee, Sushil Devkota, Hye Jeong Kim, Bomin Park and 5 more

Open access · hybridAbstract read
In one paragraph

Article in Oncogene, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.0field-weighted citation impact, top 29% 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

8 citing papers in PubMed, 13 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

15 authors at 4 institutions in 2 countries.

Jae-Il Roh *Department of Biochemistry, College of Life Science and Biotechnology, Yonsei University, Seoul, Korea.ORCID http://orcid.org/0000-0002-3956-6576
Jaehoon Lee *Department of Biochemistry, College of Life Science and Biotechnology, Yonsei University, Seoul, Korea.ORCID http://orcid.org/0000-0001-9777-5918
Young-Hoon SungDepartment of Convergence Medicine, University of Ulsan College of Medicine, Seoul, Korea.
Jahyun OhDepartment of Biochemistry, College of Life Science and Biotechnology, Yonsei University, Seoul, Korea.
Do Young HyeonDepartment of Biological Sciences, Seoul National University, Seoul, Korea.
Yujin KimDepartment of Biochemistry, College of Life Science and Biotechnology, Yonsei University, Seoul, Korea.
Seungeon LeeDepartment of Biochemistry, College of Life Science and Biotechnology, Yonsei University, Seoul, Korea.
Sushil DevkotaDepartment of Cell and Developmental Biology, University of California, San Diego, CA 92093, USA.
Hye Jeong KimDepartment of Biochemistry, College of Life Science and Biotechnology, Yonsei University, Seoul, Korea.
Bomin ParkDepartment of Biochemistry, College of Life Science and Biotechnology, Yonsei University, Seoul, Korea.
Taewook NamDepartment of Biochemistry, College of Life Science and Biotechnology, Yonsei University, Seoul, Korea.
Yaechan SongDepartment of Biochemistry, College of Life Science and Biotechnology, Yonsei University, Seoul, Korea.
Yonghwan KimDepartment of Life Systems, Sookmyung Women's University, Seoul, Korea.
Daehee HwangDepartment of Biological Sciences, Seoul National University, Seoul, Korea.
Han-Woong LeeDepartment of Biochemistry, College of Life Science and Biotechnology, Yonsei University, Seoul, Korea. hwl@yonsei.ac.kr.ORCID http://orcid.org/0000-0001-9515-3605
Yonsei University · KRSeoul National University · KRUlsan College · KRUniversity of California San Diego · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

KRAS-mutant non-small cell lung cancer (NSCLC) is a major lung cancer subtype that leads to many cancer-related deaths worldwide. Although numerous studies on KRAS-mutant type NSCLC have been conducted, new oncogenic or tumor suppressive genes need to be detected because a large proportion of NSCLC patients does not respond to currently used therapeutics. Here, we show the tumor-promoting function of a cell cycle-related protein, PIERCE1, in KRAS-mutant NSCLC. Mechanistically, PIERCE1 depletion inhibits cell growth and AKT phosphorylation (pAKT) at S473, which is particularly observed in KRAS-mutant lung cancers. Analyses of AKT-related genes using microarray, immunoblotting, and real-time quantitative PCR indicated that PIERCE1 negatively regulates the gene expression of the AKT suppressor, TRIB3, through the CHOP pathway, which is a key regulatory pathway for TRIB3 expression. Similarly, in vivo analyses of PIERCE1 depletion in the KRAS mutation-related lung cancer mouse models revealed the suppressive effect of PIERCE1 knockout in urethane- and KRAS

Indexed as

MutationSignal TransductionAnimalsBiomarkers, TumorCarcinoma, Non-Small-Cell LungCell Cycle ProteinsCell Line, TumorCell ProliferationCell Transformation, NeoplasticDisease Models, AnimalGene Expression Regulation, NeoplasticHumansLung NeoplasmsMiceMice, KnockoutModels, BiologicalBiomarkers, TumorCell Cycle ProteinsKRAS protein, humanProto-Oncogene Proteins c-aktProto-Oncogene Proteins p21(ras)RbEST47 protein, mouse

Identifiers

PMID32728173
PMCPMC7471098
OpenAlexW3045521841

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.