Evidence map›Paper›PMID 21483803›Full record

ArticlePLoS genetics2011

Cancer-associated splicing variant of tumor suppressor AIMP2/p38: pathological implication in tumorigenesis.

Jin Woo Choi, Dae Gyu Kim, Al-Eum Lee, Hye Rim Kim, Jin Young Lee, Nam Hoon Kwon, Young Kee Shin, Soon-Kyung Hwang, Seung-Hee Chang, Myung-Haing Cho and 11 more

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

47 citing papers in PubMed, 97 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. tRNA Metabolism and Lung Cancer: Beyond Translation.Frontiers in molecular biosciences · 2021
    Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Roles of Aminoacyl-tRNA Synthetases in Cancer.Frontiers in cell and developmental biology · 2020
    Review
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

21 authors at 5 institutions in 2 countries.

Jin Woo ChoiMedicinal Bioconvergence Research Center, Seoul National University, Seoul, Korea.
Dae Gyu Kim
Al-Eum Lee
Hye Rim Kim
Jin Young Lee
Nam Hoon Kwon
Young Kee Shin
Soon-Kyung Hwang
Seung-Hee Chang
Myung-Haing Cho
Yoon-La Choi
Jhingook Kim
Seung Hyun Oh
Bora Kim
Soo-Youl Kim
Hyo-Sung Jeon
Jae Yong Park
Hyunseok Peter Kang
Bum Joon Park
Jung Min Han
Sunghoon Kim
Seoul National University · KRNational Cancer Center · KRRoswell Park Comprehensive Cancer Center · USSamsung Medical Center · KRKyungpook National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although ARS-interacting multifunctional protein 2 (AIMP2, also named as MSC p38) was first found as a component for a macromolecular tRNA synthetase complex, it was recently discovered to dissociate from the complex and work as a potent tumor suppressor. Upon DNA damage, AIMP2 promotes apoptosis through the protective interaction with p53. However, it was not demonstrated whether AIMP2 was indeed pathologically linked to human cancer. In this work, we found that a splicing variant of AIMP2 lacking exon 2 (AIMP2-DX2) is highly expressed by alternative splicing in human lung cancer cells and patient's tissues. AIMP2-DX2 compromised pro-apoptotic activity of normal AIMP2 through the competitive binding to p53. The cells with higher level of AIMP2-DX2 showed higher propensity to form anchorage-independent colonies and increased resistance to cell death. Mice constitutively expressing this variant showed increased susceptibility to carcinogen-induced lung tumorigenesis. The expression ratio of AIMP2-DX2 to normal AIMP2 was increased according to lung cancer stage and showed a positive correlation with the survival of patients. Thus, this work identified an oncogenic splicing variant of a tumor suppressor, AIMP2/p38, and suggests its potential for anti-cancer target.

Indexed as

Alternative SplicingGene Expression Regulation, NeoplasticAdenocarcinomaAdenocarcinoma of LungAgedAmino Acyl-tRNA SynthetasesAnimalsApoptosisCell Line, TumorCell Transformation, NeoplasticExonsFemaleHumansLung NeoplasmsMaleMiceaminoacyl-tRNA synthetase-associated protein p38Amino Acyl-tRNA SynthetasesTumor Suppressor Protein p53

Identifiers

PMID21483803
PMCPMC3069106
OpenAlexW2046944898

What OpenQuestion 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 OpenQuestion graph.