Evidence map›Paper›PMID 26508878›Full record

ArticleOncoTargets and therapy2015

A human leucyl-tRNA synthetase as an anticancer target.

Guangwei Gao, Ying Yao, Kun Li, Dhahiri Saidi Mashausi, Dongsheng Li, Hema Negi, Suchitra Kamle, Hao Chen, Zhenghua Wu, Huchen Zhou and 1 more

Open access · goldAbstract read
In one paragraph

Article in OncoTargets and therapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.3field-weighted citation impact, top 37% 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

11 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. tRNA Function and Dysregulation in Cancer.Frontiers in cell and developmental biology · 2022
    Review
  8. Article
  9. Article
  10. Article
  11. 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

11 authors at 1 institution in 1 country.

Guangwei GaoSchool of Pharmacy, Shanghai Jiao Tong University, Shanghai, People's Republic of China.
Ying YaoSchool of Pharmacy, Shanghai Jiao Tong University, Shanghai, People's Republic of China.
Kun LiSchool of Pharmacy, Shanghai Jiao Tong University, Shanghai, People's Republic of China.
Dhahiri Saidi MashausiSchool of Pharmacy, Shanghai Jiao Tong University, Shanghai, People's Republic of China.
Dongsheng LiSchool of Pharmacy, Shanghai Jiao Tong University, Shanghai, People's Republic of China.
Hema NegiSchool of Pharmacy, Shanghai Jiao Tong University, Shanghai, People's Republic of China.
Suchitra KamleSchool of Pharmacy, Shanghai Jiao Tong University, Shanghai, People's Republic of China.
Hao ChenSchool of Pharmacy, Shanghai Jiao Tong University, Shanghai, People's Republic of China.
Zhenghua WuSchool of Pharmacy, Shanghai Jiao Tong University, Shanghai, People's Republic of China.
Huchen ZhouSchool of Pharmacy, Shanghai Jiao Tong University, Shanghai, People's Republic of China.
Dawei LiSchool of Pharmacy, Shanghai Jiao Tong University, Shanghai, People's Republic of China.
Shanghai Jiao Tong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Several aminoacyl-tRNA synthetases have been reported to be overexpressed for charging essential aminoacyl-tRNAs in many cancer types. In this study, we aimed to explore the potential role of leucyl-tRNA synthetase (LARS) as an anticancer target. MTT assay was performed to screen inhibitors to human LARS (hsLARS) from compounds AN2690 and its derivatives, compounds 1-6, in U2OS and SKOV3 cells. The compound with the strongest inhibitory ability was further investigated for its inhibitory effect in cancer cell lines and in an animal tumor model. Additionally, a LARS-rescue experiment was performed to explore the potential target in U2OS using Western blot and flow cytometry. Luciferase reporter assay was designed to analyze the effect of of hsLARS inhibitor on p21 activation. We identified an hsLARS inhibitor (compound 2) that suppressed the proliferation of U2OS and SKOV3 cells in vitro. A LARS-rescue experiment demonstrated that the proliferation inhibition was induced by targeting intracellular LARS. In addition, the hsLARS inhibition was shown to activate the p21 early transcription and promote cell apoptosis, as well as reduce implanted EMT6 tumor progression in mice. Our results suggest that LARS might serve as a potential anticancer target through the p21 signaling pathway and that the nutritional signaling pathway may provide a valuable anticancer strategy for further investigation.

Indexed as

anticancer targetapoptosisleucyl-tRNA synthetasemouse model

Identifiers

PMID26508878
PMCPMC4610879
OpenAlexW2176868705

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.