Evidence map›Paper›PMID 35740562›Full record

ReviewCancers2022

Acetyl-CoA Synthetase 2 as a Therapeutic Target in Tumor Metabolism.

Mengfang Liu, Na Liu, Jinlei Wang, Shengqiao Fu, Xu Wang, Deyu Chen

Open access · goldAbstract readReview
In one paragraph

Review in Cancers, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
2.8field-weighted citation impact, top 8% 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

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Exploring metabolic signatures in urine using NMR for improved prognosis of gliomas.Metabolomics : Official journal of the Metabolomic Society · 2026
    Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. Application of Metabolic Reprogramming to Cancer Imaging and Diagnosis.International journal of molecular sciences · 2022
    Review
  17. Review
  18. 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

6 authors at 2 institutions in 1 country.

Mengfang LiuInstitute of Oncology, Affiliated Hospital of Jiangsu University, 438 Jiefang Road, Zhenjiang 212001, China.
Na LiuInstitute of Oncology, Affiliated Hospital of Jiangsu University, 438 Jiefang Road, Zhenjiang 212001, China.
Jinlei WangInstitute of Oncology, Affiliated Hospital of Jiangsu University, 438 Jiefang Road, Zhenjiang 212001, China.
Shengqiao FuInstitute of Oncology, Affiliated Hospital of Jiangsu University, 438 Jiefang Road, Zhenjiang 212001, China.
Xu WangInstitute of Oncology, Affiliated Hospital of Jiangsu University, 438 Jiefang Road, Zhenjiang 212001, China.
Deyu ChenInstitute of Oncology, Affiliated Hospital of Jiangsu University, 438 Jiefang Road, Zhenjiang 212001, China.
Jiangsu University · CNAffiliated Hospital of Jiangsu University · CN

Funding

the Jiangsu Provincial Science and Technology Supporting Program BE2017696the Medical Innovation Team of Jiangsu Province CXTDC2016009the National Natural Science Foundation of China 81572956the National Natural Science Foundation of China 81701945Zhenjiang Key Research and Development Program SH2020067
6 · The paper itself

Abstract

Acetyl-CoA Synthetase 2 (ACSS2) belongs to a member of the acyl-CoA short-chain synthase family, which can convert acetate in the cytoplasm and nucleus into acetyl-CoA. It has been proven that ACSS2 is highly expressed in glioblastoma, breast cancer, liver cancer, prostate cancer, bladder cancer, renal cancer, and other tumors, and is closely related to tumor stage and the overall survival rate of patients. Accumulating studies show that hypoxia and a low serum level induce ACSS2 expression to help tumor cells cope with this nutrient-poor environment. The potential mechanisms are associated with the ability of ACSS2 to promote the synthesis of lipids in the cytoplasm, induce the acetylation of histones in the nucleus, and facilitate the expression of autophagy genes. Novel-specific inhibitors of ACSS2 are developed and confirmed to the effectiveness in pre-clinical tumor models. Targeting ACSS2 may provide novel approaches for tumor treatment. This review summarizes the biological function of ACSS2, its relation to survival and prognosis in different tumors, and how ACSS2 mediates different pathways to promote tumor metastasis, invasion, and drug resistance.

Indexed as

ACSS2inhibitormetabolismtargeted therapytumor

Identifiers

PMID35740562
PMCPMC9221533
OpenAlexW4282590239

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.