Coordinated methyl readers: Functional communications in cancer

Il Geun Park, Minsol Jeon, Hyunkyung Kim, Ji Min Lee

Research output: Contribution to journalReview articlepeer-review

9 Citations (Scopus)


Methylation is a major post-translational modification (PTM) generated by methyltransferase on target proteins; it is recognized by the epigenetic reader to expand the functional diversity of proteins. Methylation can occur on specific lysine or arginine residues localized within regulatory domains in both histone and nonhistone proteins, thereby allowing distinguished properties of the targeted protein. Methylated residues are recognized by chromodomain, malignant brain tumor (MBT), Tudor, plant homeodomain (PHD), PWWP, WD-40, ADD, and ankyrin repeats by an induced-fit mechanism. Methylation-dependent activities regulate distinct aspects of target protein function and are largely reliant on methyl readers of histone and nonhistone proteins in various diseases. Methylation of nonhistone proteins that are recognized by methyl readers facilitates the degradation of unwanted proteins, as well as the stabilization of necessary proteins. Unlike nonhistone substrates, which are mainly monomethylated by methyltransferase, histones are di- or trimethylated by the same methyltransferases and then connected to other critical regulators by methyl readers. These fine-tuned controls by methyl readers are significant for the progression or inhibition of diseases, including cancers. Here, current knowledge and our perspectives about regulating protein function by methyl readers are summarized. We also propose that expanded research on the strong crosstalk mechanisms between methylation and other PTMs via methyl readers would augment therapeutic research in cancer.

Original languageEnglish
Pages (from-to)88-99
Number of pages12
JournalSeminars in Cancer Biology
Publication statusPublished - 2022 Aug

Bibliographical note

Funding Information:
This work was supported by Samsung Research Funding & Incubation Center of Samsung Electronics under Project Number [SRFC-MA2002-07]; Basic Science Research Program [NRF-2021R1C1C1008780 to J.M.L. NRF-2020R1C1C1010489 to H.K.] from the National Research Foundation (NRF) grant funded by the Korean government (MSIT); Korea University Medical Center Grant [K1925011 to H.K.]. The figures were generated using BioRender with a paid license to publish.

Publisher Copyright:
© 2021 The Author(s)


  • Chromodomain
  • Epigenetics
  • Methyl reader
  • PHD
  • Tudor

ASJC Scopus subject areas

  • Cancer Research


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