Evidence map›Paper›PMID 38426936›Full record

ArticleJournal of cellular and molecular medicine2024

SIRT2-mediated deacetylation of ACLY promotes the progression of oesophageal squamous cell carcinoma.

Xueying Zhang, Yue Xu, Shenglei Li, Yue Qin, Guangzhao Zhu, Qing Zhang, Yanting Zhang, Fangxia Guan, Tianli Fan, Hongtao Liu

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

12 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. Review
  8. Review
  9. The role of acetylation and deacetylation in cancer metabolism.Clinical and translational medicine · 2025
    Review
  10. Article
  11. Article
  12. 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

10 authors at 3 institutions in 1 country.

Xueying ZhangSchool of Life Sciences, Zhengzhou University, Zhengzhou, Henan, China.
Yue XuDepartment of Pathology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.
Shenglei LiDepartment of Pathology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.
Yue QinSchool of Life Sciences, Zhengzhou University, Zhengzhou, Henan, China.
Guangzhao ZhuSchool of Life Sciences, Zhengzhou University, Zhengzhou, Henan, China.
Qing ZhangTranslational Medicine Research Center, Zhengzhou People's Hospital, Zhengzhou, Henan, China.
Yanting ZhangSchool of Life Sciences, Zhengzhou University, Zhengzhou, Henan, China.
Fangxia GuanSchool of Life Sciences, Zhengzhou University, Zhengzhou, Henan, China.
Tianli FanDepartment of Pharmacology, School of Basic Medicine, Zhengzhou University, Zhengzhou, Henan, China.
Hongtao LiuSchool of Life Sciences, Zhengzhou University, Zhengzhou, Henan, China.ORCID 0000-0003-3162-0029
Zhengzhou University · CNFirst Affiliated Hospital of Zhengzhou University · CNZhengzhou People's Hospital · CN

Funding

Central Plains Thousand People Plan of Henan Province 204200510013Discipline Innovation and Wisdom Introduction Plan of Higher Education in Henan Province CXJD2021002Joint Construction Project of Henan Medical Science and Technology Research Program LHGJ20210701Key Discipline Construction Project for Prevention and Treatment of Esophageal Cancer in Zhengzhou University XKZDJC202001Key project of Henan Provincial Science and Technology Research and Development Joint Fund 225200810011National Natural Science Foundation of China 81272691National Natural Science Foundation of China 82073084Natural Science Foundation of Henan Province 202300410404
6 · The paper itself

Abstract

ATP citrate lyase (ACLY), as a key enzyme in lipid metabolism, plays an important role in energy metabolism and lipid biosynthesis of a variety of tumours. Many studies have shown that ACLY is highly expressed in various tumours, and its pharmacological or gene inhibition significantly inhibits tumour growth and progression. However, the roles of ACLY in oesophageal squamous cell carcinoma (ESCC) remain unclear. Here, our data showed that ACLY inhibitor significantly attenuated cell proliferation, migration, invasion and lipid synthesis in different ESCC cell lines, whereas the proliferation, migration, invasion and lipid synthesis of ESCC cells were enhanced after ACLY overexpression. Furthermore, ACLY inhibitor dramatically suppressed tumour growth and lipid metabolism in ESCC cells xenografted tumour model, whereas ACLY overexpression displayed the opposite effect. Mechanistically, ACLY protein harboured acetylated modification and interacted with SIRT2 protein in ESCC cells. The SIRT2 inhibitor AGK2 significantly increased the acetylation level of ACLY protein and inhibited the proliferation and migration of ESCC cells, while overexpression of ACLY partially reversed the inhibitory effect of AGK2 on ESCC cells. Overall, these results suggest that targeting the SIRT2/ACLY signalling axis may be a potential therapeutic strategy for ESCC patients.

Indexed as

Esophageal NeoplasmsEsophageal Squamous Cell CarcinomaATP Citrate (pro-S)-LyaseCell Line, TumorCell ProliferationGene Expression Regulation, NeoplasticHumansLipidsSirtuin 2ATP Citrate (pro-S)-LyaseLipidsSIRT2 protein, humanSirtuin 2acetylationATP citrate lyaseBMS-303141lipid metabolismoesophageal squamous cell carcinomasirtuin 2

Identifiers

PMID38426936
PMCPMC10906381
OpenAlexW4392359487

What OpenQuestion holds

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LicenceCC BY
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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.