Evidence map›Paper›PMID 35371279›Full record

ArticleComputational and mathematical methods in medicine2022

Expression and Regulation Network of HDAC3 in Acute Myeloid Leukemia and the Implication for Targeted Therapy Based on Multidataset Data Mining.

Minhua Li, Feifei Lan, Chen Li, Ning Li, Xiaojie Chen, Yueyuan Zhong, Yue Yang, Yingqi Shao, Yi Kong, Xinming Li and 5 more

RetractedOpen access · hybridAbstract readRetracted Publication
In one paragraph

Article in Computational and mathematical methods in medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.5field-weighted citation impact, top 39% 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

6 citing papers in PubMed, 7 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors at 4 institutions in 2 countries.

Minhua LiSchool of Laboratory Medicine, Hangzhou Medical College, Hangzhou, China.
Feifei LanMedical Genetics Center, Guangdong Women and Children Hospital, Guangzhou, China.
Chen LiDepartment of Biology, Chemistry, Pharmacy, Free University of Berlin, 14195 Berlin, Germany.ORCID https://orcid.org/0000-0002-6895-2759
Ning LiZhu's Group, Guangdong Medical University, Zhanjiang, China.
Xiaojie ChenZhu's Group, Guangdong Medical University, Zhanjiang, China.
Yueyuan ZhongZhu's Group, Guangdong Medical University, Zhanjiang, China.
Yue YangZhu's Group, Guangdong Medical University, Zhanjiang, China.
Yingqi ShaoZhu's Group, Guangdong Medical University, Zhanjiang, China.
Yi KongZhu's Group, Guangdong Medical University, Zhanjiang, China.
Xinming LiZhu's Group, Guangdong Medical University, Zhanjiang, China.
Danny WuZhu's Group, Guangdong Medical University, Zhanjiang, China.
Jingyu ZhangZhu's Group, Guangdong Medical University, Zhanjiang, China.
Wenqing ChenZhu's Group, Guangdong Medical University, Zhanjiang, China.
Zesong LiThe First Affiliated Hospital of Shenzhen University, Shenzhen Second People's Hospital (Shenzhen Institute of Translational Medicine), Shenzhen, China.ORCID https://orcid.org/0000-0003-0975-4434
Xiao ZhuSchool of Laboratory Medicine, Hangzhou Medical College, Hangzhou, China.ORCID https://orcid.org/0000-0002-1737-3386
Guangdong Medical College · CNFreie Universität Berlin · DEGuangdong Province Women and Children Hospital · CNShenzhen Second People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Histone deacetylase 3 (HDAC3) plays an important role in the development and progression of a variety of cancers, but its regulatory mechanism in acute myeloid leukemia (LAML) is not entirely understood. Methods: We analyzed the expression of HDAC3 in normal and cancerous tissues using Oncomine, UALCAN, and GEO databases. Changes of the HDAC3 gene were analyzed by cBioPortal. The genes coexpressed with HDAC3 were analyzed by WebGestalt, and the predicted signaling pathways in KEGG were discussed. Results: We discovered that the expression of HDAC3 was elevated in some types of acute myeloid leukemia. The HDAC3 gene has a strong positive correlation with SLC25A5, NDUFA2, Cox4I1, and EIF3K, which regulate cell growth and development. HDAC3 transcription is higher in patients with FLT3 mutation than in healthy people. HDAC3 can be directly involved in regulating the thyroid hormone signaling pathway. MEF2D is directly involved in the cGMP-PKG signaling pathway, and the HDAC3 gene has a strong synergistic relationship with MEF2D. HDAC3 is indirectly involved in the cGMP-PKG signaling pathway, thereby indirectly regulating the expression levels of p53 and p21 genes in patients with LAML. Genomics of Drug Sensitivity in Cancer (GDSC) database analysis revealed that the application of the HDAC3 inhibitor can inhibit the proliferation of leukemia cells. Conclusions: Therefore, our data suggest that HDAC3 may be a possible therapeutic target for acute myeloid leukemia.

Indexed as

Histone DeacetylasesLeukemia, Myeloid, AcuteData MiningHistone Deacetylase 3HumansSignal TransductionHistone Deacetylase 3Histone Deacetylases

Identifiers

PMID35371279
PMCPMC8966751
OpenAlexW4221131979

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.