Evidence map›Paper›PMID 34400610›Full record

ArticleSignal transduction and targeted therapy2021

Glucose-sensitive acetylation of Seryl tRNA synthetase regulates lipid synthesis in breast cancer.

Jin Zhao, Hangming Bai, Xiaoyu Li, Jie Yan, Gengyi Zou, Longlong Wang, Xiru Li, Ze Liu, Rong Xiang, Xiang-Lei Yang and 1 more

Open access · goldAbstract read
In one paragraph

Article in Signal transduction and targeted therapy, 2021. 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
1.4field-weighted citation impact, top 19% 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.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Seryl-tRNA synthetase inhibits Wnt signaling and breast cancer progression and metastasis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  8. Article
  9. METTL5 promotes gastric cancer progressionWorld journal of gastrointestinal oncology · 2024
    Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. tRNA Function and Dysregulation in Cancer.Frontiers in cell and developmental biology · 2022
    Review
  16. 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 2 institutions in 2 countries.

Jin ZhaoSchool of Medicine, Nankai University, Tianjin, China.
Hangming BaiSchool of Medicine, Nankai University, Tianjin, China.
Xiaoyu LiSchool of Medicine, Nankai University, Tianjin, China.
Jie YanSchool of Medicine, Nankai University, Tianjin, China.
Gengyi ZouSchool of Medicine, Nankai University, Tianjin, China.
Longlong WangSchool of Medicine, Nankai University, Tianjin, China.
Xiru LiDepartment of General Surgery, Chinese PLA General Hospital, Beijing, China.
Ze LiuThe Scripps Research Institute, La Jolla, CA, USA.
Rong XiangSchool of Medicine, Nankai University, Tianjin, China.ORCID 0000-0003-3487-7348
Xiang-Lei YangThe Scripps Research Institute, La Jolla, CA, USA.
Yi ShiSchool of Medicine, Nankai University, Tianjin, China. yishi@nankai.edu.cn.ORCID 0000-0003-2530-410X
Nankai University · CNScripps Research Institute · US

Funding

Exploring the Functions of tRNA Synthetases in the Nucleus and their Relationship to CMTR01NS113583 · NINDS · SCRIPPS RESEARCH INSTITUTE, THE · PI BURGESS, ROBERT W., YANG, XIANG-LEI · 2020 to 2024
$2.9M
NINDS NIH HHS R01 NS113583
6 · The paper itself

Abstract

Abnormally enhanced de novo lipid biosynthesis has been increasingly realized to play crucial roles in the initiation and progression of varieties of cancers including breast cancer. However, the mechanisms underlying the dysregulation of lipid biosynthesis in breast cancer remain largely unknown. Here, we reported that seryl tRNA synthetase (SerRS), a key enzyme for protein biosynthesis, could translocate into the nucleus in a glucose-dependent manner to suppress key genes involved in the de novo lipid biosynthesis. In normal mammary gland epithelial cells glucose can promote the nuclear translocation of SerRS by increasing the acetylation of SerRS at lysine 323. In SerRS knock-in mice bearing acetylation-defective lysine to arginine mutation, we observed increased body weight and adipose tissue mass. In breast cancer cells the acetylation and nuclear translocation of SerRS are greatly inhibited. Overexpression of SerRS, in particularly the acetylation-mimetic lysine to glutamine mutant, dramatically inhibits the de novo lipid synthesis and hence greatly suppresses the proliferation of breast cancer cells and the growth of breast cancer xenografts in mice. We further identified that HDAC4 and HDAC5 regulated the acetylation and nuclear translocation of SerRS. Thus, we identified a SerRS-meditated inhibitory pathway in glucose-induced lipid biosynthesis, which is dysregulated in breast cancer.

Indexed as

AcetylationActive Transport, Cell NucleusAdipose TissueAmino Acid SequenceAnimalsBreast NeoplasmsFemaleGene Expression Regulation, NeoplasticGene Knock-In TechniquesGlucoseHeterograftsHistone DeacetylasesHumansLipidsMiceSerine-tRNA LigaseGlucoseHdac5 protein, mouseHistone DeacetylasesLipidsSerine-tRNA Ligase

Identifiers

PMID34400610
PMCPMC8368063
OpenAlexW3195596607

What OpenQuestion holds

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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.