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Cited by 51Wnt/β-catenin signaling in development and cancerHistone Deacetylase Inhibitors ResearchEpigenetics and DNA Methylation

The interaction of canonical Wnt/β-catenin signaling with protein lysine acetylation

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You, Hongjuan, Li, Qi, Kong, Delong, Liu, Xiangye, Kong, Fanyun, Zheng, Kuiyang, Tang, Renxian·2022·Cellular & Molecular Biology Letters
DOI 10.1186/s11658-021-00305-5PMC PMC8903542
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Abstract

Canonical Wnt/β-catenin signaling is a complex cell-communication mechanism that has a central role in the progression of various cancers. The cellular factors that participate in the regulation of this signaling are still not fully elucidated. Lysine acetylation is a significant protein modification which facilitates reversible regulation of the target protein function dependent on the activity of lysine acetyltransferases (KATs) and the catalytic function of lysine deacetylases (KDACs). Protein lysine acetylation has been classified into histone acetylation and non-histone protein acetylation. Histone acetylation is a kind of epigenetic modification, and it can modulate the transcription of important biological molecules in Wnt/β-catenin signaling. Additionally, as a type of post-translational modification, non-histone acetylation directly alters the function of the core molecules in Wnt/β-catenin signaling. Conversely, this signaling can regulate the expression and function of target molecules based on histone or non-histone protein acetylation. To date, various inhibitors targeting KATs and KDACs have been discovered, and some of these inhibitors exert their anti-tumor activity via blocking Wnt/β-catenin signaling. Here, we discuss the available evidence in understanding the complicated interaction of protein lysine acetylation with Wnt/β-catenin signaling, and lysine acetylation as a new target for cancer therapy via controlling this signaling.

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  • Inhibition of class I HDACs is associated with activation of Wnt/β-catenin signaling.

    “It has been demonstrated that inhibition of class I HDACs is associated with activation of Wnt/β-catenin signaling [42–47].”

    From CI-994 is a dual modulator of class I HDACs and Wnt/β-catenin signaling for the treatment of Alzheimer's disease (2026) · cites this paper as [45]

    The section “Targeting protein acetylation to suppress Wnt/β-catenin signaling” (page unavailable) says that mocetinostat, an inhibitor of class I and IV HDACs, suppresses Wnt/β-catenin signaling. Although the paper also describes HDAC1 and HDAC2 as repressors of Wnt-dependent transcription, its stated effect of an HDAC inhibitor is contrary to the claimed activation. (LLM, conf=0.86)

    Checked by a reasoning model — may be wrong.

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  • In the absence of Wnt signaling, HDAC1 and HDAC2 bind to TCF/LEF, cause histone H3 hypo-acetylation at the promoters of Wnt-dependent genes and consequent inhibition of Wnt target gene expression.

    “Fifthly, in the absence of Wnt signaling, HDAC1 and HDAC2 bind to TCF/LEF, cause histone H3 hypo-acetylation at the promoters of Wnt-dependent genes and consequent inhibition of Wnt target gene expression [45, 46].”

    From CI-994 is a dual modulator of class I HDACs and Wnt/β-catenin signaling for the treatment of Alzheimer's disease (2026) · cites this paper as [45]

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Cited by

Sorted by citations

Authors
You, H., Li, Q., Kong, D., Liu, X., Kong, F., Zheng, K., & Tang, R.
Affiliations
Xuzhou Medical College (CN)
Corresponding author
  • Kong, Fanyun
  • Tang, Renxian
ORCID
Venue
Cellular & Molecular Biology Letters
Publisher
Springer Science and Business Media LLC
Published
2022-01-15
Volume
27
Issue
1
Pages
7-7
ISSN
  • 1425-8153 (ISSN-L)
  • 1689-1392
DOI
10.1186/s11658-021-00305-5
PMC
PMC8903542
OpenAlex
W4206474828
Cited by
51
References
2
Citations by year
2026: 8 · 2025: 9 · 2024: 7 · 2023: 18 · 2022: 9
FWCI
3.76
Type
journal article
Language
en
Open access
Licence
Locations
  • Cellular & Molecular Biology Letters (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
  • Priority Academic Program Development of Jiangsu Higher Education Institutions (PAPD)
  • Natural Science Foundation of Jiangsu Province (BK20211347)
  • Xuzhou Technology Bureau Foundation (KC21065)
  • Natural Science Foundation of the Jiangsu Higher Education Institutions (21KJA310004)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Wnt/β-catenin signaling in development and cancer
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Histone Deacetylase Inhibitors Research
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
Keywords
Wnt/β-catenin signaling, lysine acetylation, histone acetyltransferase, lysine deacetylases, histone acetylation, non-histone protein acetylation, post-translational modification, epigenetic regulation, cancer therapy targets, anticancer activity
MeSH terms
Acetylation, Lysine, Protein Processing, Post-Translational, beta Catenin, Wnt Signaling Pathway

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