Last update 01 Nov 2024

SUZ12

Last update 01 Nov 2024

Basic Info

Synonyms

ChET 9 protein, CHET9, Chromatin precipitated E2F target 9 protein

+ [7]

Introduction

Polycomb group (PcG) protein. Component of the PRC2 complex, which methylates 'Lys-9' (H3K9me) and 'Lys-27' (H3K27me) of histone H3, leading to transcriptional repression of the affected target gene (PubMed:15225548, PubMed:15231737, PubMed:15385962, PubMed:16618801, PubMed:17344414, PubMed:18285464, PubMed:28229514, PubMed:29499137, PubMed:31959557). The PRC2 complex may also serve as a recruiting platform for DNA methyltransferases, thereby linking two epigenetic repression systems (PubMed:12435631, PubMed:12351676, PubMed:15385962, PubMed:15099518, PubMed:15225548, PubMed:15684044, PubMed:16431907, PubMed:18086877, PubMed:18285464). Genes repressed by the PRC2 complex include HOXC8, HOXA9, MYT1 and CDKN2A (PubMed:15231737, PubMed:16618801, PubMed:17200670, PubMed:31959557).

Drugs associated with SUZ12

E-3P-MDM2

Target

EED x EZH2 x SUZ12

Mechanism

EED inhibitors [+2]

Active Org.

Shenyang Pharmaceutical University [+1]

Originator Org.

Shenyang Pharmaceutical University [+1]

Active Indication

Lymphoma

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

UNC6846

Target

EED x EZH2 x SUZ12

Mechanism

EED inhibitors [+2]

Active Org.-

Originator Org.-

Active Indication-

Inactive Indication-

Drug Highest Phase-

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

UNC6851

Target

EED x EZH2 x SUZ12

Mechanism

EED inhibitors [+2]

Active Org.-

Originator Org.-

Active Indication-

Inactive Indication-

Drug Highest Phase-

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with SUZ12

100 Translational Medicine associated with SUZ12

0 Patents (Medical) associated with SUZ12

735

Literatures (Medical) associated with SUZ12

01 Oct 2024·Clinical Genetics

EZH2‐associated tumor malignancy: A prominent target for cancer treatment

Review

Author: Biray‐Avci, Cigir ; Sabour‐Takanlou, Maryam ; Sabour‐Takanlou, Leila

AbstractThe discussion in this review centers around the significant relationships between EZH2 and the initiation, progression, metastasis, metabolism, drug resistance, and immune regulation of cancer. Polycomb group (PcG) proteins, which encompass two primary Polycomb repressor complexes (PRC1 and PRC2), have been categorized. PRC2 consists mainly of four subunits, namely EZH2, EED, SUZ12, and RbAp46/48. As the crucial catalytic component within the PRC2 complex, EZH2 plays a pivotal role in controlling a wide range of biological processes. Overexpression/mutations of EZH2 have been detected in a wide variety of tumors. Several mechanisms of EZH regulation have been identified, including regulation EZH2 mRNA by miRNAs, LncRNAs, accessibility to DNA via DNA‐binding proteins, post‐translational modifications, and transcriptional regulation. EZH2 signaling triggers cancer progression and may intervene with anti‐tumor immunity; therefore it has charmed attention as an effective therapeutic target in cancer therapy. Numerous nucleic acid‐based therapies have been used in the modification of EZH2. In addition to gene therapy approaches, pharmaceutical compounds can be used to target the EZH2 signaling pathway in the treatment of cancer. EZH2‐associated tumor cells and immune cells enhance the effects of the immune response in a variety of human malignancies. The combination of epigenetic modifying agents, such as anti‐EZH2 compounds with immunotherapy, could potentially be efficacious even in the context of immunosuppressive tumors. Summary, understanding the mechanisms underlying resistance to EZH2 inhibitors may facilitate the development of novel drugs to prevent or treat relapse in treated patients.

01 Oct 2024·Cancer Medicine

The expression and role of SUZ12 in lung adenocarcinoma

Article

Author: Hu, Xingsheng ; Zhong, Ping ; Hu, Chunhong

AbstractBackgroundSUZ12 is one of the core members of the polycomb repressive complex 2 (PRC2), but its expression and role in lung adenocarcinoma (LUAD) are unclear. We aimed to explore the expression, prognosis, biological functions and roles of SUZ12 in LUAD.MethodsThe expression of SUZ12 was detected by immunohistochemical staining, qRT‐PCR, and western blotting in LUAD tissues and cells. The biological functions and molecular mechanisms of SUZ12 were characterized by a range of in vitro and in vivo experiments.ResultsSUZ12 was overexpressed in LUAD tissues, and high SUZ12 expression was correlated with worse clinicopathological features and a poorer prognosis. Knockdown of SUZ12 significantly inhibited cell growth, colony formation, invasion, and migration, and induced apoptosis and G1/S phase arrest, while overexpression of SUZ12 had the opposite effects. Knockdown of SUZ12 decreased the tumorigenic capacity of A549 cells in vivo. The expression of key signaling molecules related to the cell cycle, apoptosis, migration, and immunity were altered by the knockdown or overexpression of SUZ12. SUZ12 can directly bind to the Bax promoter region, EZH2 and H3K27me3 levels dependents on SUZ12. The expression levels of SUZ12 and Bax were negatively correlated in LUAD tissues.ConclusionsSUZ12 is a new oncogene related to the poor prognosis of LUAD. SUZ12 regulates LUAD progression by regulating the expression of related signaling molecules, and as a part of the PRC2 complex, it may bind to the Bax promoter to silence Bax expression.

01 Oct 2024·American Journal of Medical Genetics Part A

Biallelic loss‐of‐function variants of EZH1 cause a novel developmental disorder with central precocious puberty

Article

Author: Yanagi, Kumiko ; Okamoto, Nobuhiko ; Kaname, Tadashi ; Ogitani, Ayako ; Yoshida, Sayaka ; Etani, Yuri

AbstractPathogenic variants of polycomb repressive complex‐2 (PRC2) subunits are associated with overgrowth syndromes and neurological diseases. EZH2 is a major component of PRC2 and mediates the methylation of H3K27 trimethylation (H3K27me3). Germline variants of EZH2 have been identified as a cause of Weaver syndrome (WS), an overgrowth/intellectual disability (OGID) syndrome characterized by overgrowth, macrocephaly, accelerated bone age, intellectual disability (ID), and characteristic facial features. Germline variants of SUZ12 and EED, other components of PRC2, have also been reported in the WS or Weaver‐like syndrome. EZH1 is a homolog of EZH2 that interchangeably associates with SUZ12 and EED. Recently, pathogenic variants of EZH1 have been reported in individuals with dominant and recessive neurodevelopmental disorders. We herein present sisters with biallelic loss‐of‐function variants of EZH1. They showed developmental delay, ID, and central precocious puberty, but not the features of WS or other OGID syndromes.

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SUZ12

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