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Last update 08 May 2025

ANAPC

Last update 08 May 2025

Basic Info

Synonyms

APC/C, cyclosome

Introduction-

Drugs associated with ANAPC

APC1 (TwoToBiotech)

Target

ANAPC1 x INSR

Mechanism

ANAPC1 modulators [+1]

Active Org.

TwoToBiotech

Originator Org.

TwoToBiotech

Active Indication

Diabetes Mellitus, Type 2

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

WO2022129397

Patent Mining

Target

ANAPC

Mechanism-

Active Org.

Oxford Brookes University [+1]

Originator Org.

Oxford Brookes University [+1]

Active Indication

Neoplasms

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with ANAPC

100 Translational Medicine associated with ANAPC

0 Patents (Medical) associated with ANAPC

2,044

Literatures (Medical) associated with ANAPC

31 Dec 2025·Future Science OA

Elevated expression of ANAPC1 in lung squamous cell carcinoma: clinical implications and mechanisms

Article

Author: Chi, Bang-Teng ; Wei, Yue ; Song, Chang ; Zhao, Chun-Yan ; He, Shu-Jia ; Lu, Hui-Ping ; Chen, Gang ; Kong, Jin-Liang ; He, Rong-Quan ; Huang, Wan-Ying ; Chen, Xiao-Song ; Chen, Yi-Yang ; Chen, Feng

AIMTo investigate the comprehensive expression levels and possible molecular mechanisms of Anaphase Promoting Complex Subunit 1 (ANAPC1) in lung squamous cell carcinoma (LUSC).METHODSData from 2,031 samples were combined to evaluate ANAPC1 mRNA levels, and 118 samples were collected for immunohistochemical (IHC) analysis. High-expression co-expressed genes (HECEGs) associated with ANAPC1 were analyzed for signaling pathways. Clinical significance, immune computations, and Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR) validation of ANAPC1's role in LUSC were assessed. Molecular docking evaluated binding affinity with potential therapeutics.RESULTSANAPC1 mRNA was significantly upregulated in LUSC (SMD = 1.97, 95% CI [1.26-2.67]). Protein-level analysis confirmed this upregulation (p < 0.001). Most HECEGs associated with ANAPC1 were enriched in cell cycle pathways. Higher ANAPC1 expression correlated with poorer survival in LUSC patients (HR = 1.11, 95% CI: 1-1.49). ANAPC1 expression was higher in males and N1-stage vs. females and N0-stage; lower in grade I vs. II/III. Overexpression reduces immune cell infiltration and immunotherapy effectiveness, while knockdown inhibits cell proliferation. Drug sensitivity and docking analyses identified tenovin-1, carboxyatractyloside, and phycocyanobilin as potential antitumor agents targeting ANAPC1.CONCLUSIONThe elevated expression of ANAPC1 might play a role in LUSC advancement and progression through its participation in cell growth-related pathways.

01 Jul 2025·Plant Science

Studies on the regulation of E3 ubiquitin ligase APC3 and its interacting proteins on the tetraspore formation and release in Gracilariopsis lemaneiformis (Rhodophyta)

Article

Author: Chen, Rui ; Zhang, Jingyu ; Wang, Lu ; Yin, Jingru ; Wu, Qiong ; Jiang, Min ; Sui, Zhenghong

E3 ubiquitin ligases play significant roles in development of high plants and animals. We recently found that E3 ubiquitin ligase APC3, the subunit of the anaphase promoting complex/cyclosome, was involved in tetraspore formation and release in Gracilariopsis lemaneiformis, an economically important red alga. GlAPC3 showed opposite expression pattern in low-fertility cultivar 981 and high-fertility strain WLP during the process of tetraspore formation and release, up-regulated in 981 and down-regulated in WLP. Five proteins related to chromosome segregation, SMC3, NUF2, APC2, APC8 and APC10, were detected to interact with APC3, which were all located in the nucleus. NUF2 and CDC20 were the substrates of APC3, combined with Lysine-11, Lysine-48 and Lysine-63 of ubiquitin chains containing two or four ubiquitin. The key amino acids for ubiquitination of APC3 covered 474th Aspartate, 502nd tyrosine and 506th leucine, any mutation of which resulted in a loss of ubiquitination. During the process of tetraspore formation and release, SMC3 was significantly up-regulated only in 981, low number of tetraspore release. NUF2 and APC2 were significantly down-regulated only in WLP, with high frequency and large amount of tetraspores release. The data provided that APC3, SMC3 and NUF2 might be the key gene affecting the fertility of Gp. lemaneiformis. The study helps to explore the regulation mechanism of APC3 with SMC3 and NUF2 by the process of chromatids segregation in regulating tetraspore formation and release of Gp. lemaneiformis.

01 Jul 2025·Cancer Letters

The m6A hypermethylation-induced PIR overexpression regulates H3K4me3 and promotes tumorigenesis of uveal melanoma

Article

Author: Chen, Ying ; Tian, Hao ; Jia, Ruobing ; Dong, Xiaokang ; Fan, Xianqun

Uveal melanoma (UM) is the most common primary ocular malignancy in adults, characterized by high mortality, strong metastatic potential, and limited treatment options, necessitating the identification of novel therapeutic targets. Here, we identified Pirin (PIR) as a key oncogenic factor in UM through comprehensive multi-omics analyses, revealing that PIR is significantly upregulated and correlates with poor prognosis. Functional assays indicated that inhibiting PIR markedly suppressed UM progression, highlighting its critical role in tumorigenesis behavior. Mechanistically, PIR expression is driven by aberrant N6-methyladenosine (m⁶A) modifications mediated by METTL3 and IGF2BP3. Meanwhile, the high expressed PIR acts as a transcriptional co-regulator by interacting with WDR5, resulting in the regulation of H3K4me3 modifications at the ANAPC10 promoter region and subsequent promotion of ANAPC10 expression. Overall, our study uncovered the METTL3/IGF2BP3 (m6A)-PIR-WDR5 (H3K4me3)-ANAPC10 axis, bridging RNA methylation and histone methylation in UM pathogenesis. By unmasking these intricate epigenetic interactions, we provided novel insights into UM biology and identified potential therapeutic targets for tumor treatment, offering the theoretical support for future drug development and clinical applications.

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ANAPC

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