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Last update 08 May 2025

NUF2

Last update 08 May 2025

Basic Info

Synonyms

CDCA1, Cell division cycle-associated protein 1, CT106

+ [7]

Introduction

Acts as a component of the essential kinetochore-associated NDC80 complex, which is required for chromosome segregation and spindle checkpoint activity (PubMed:12438418, PubMed:14654001, PubMed:15062103, PubMed:15235793, PubMed:15239953, PubMed:15548592, PubMed:17535814). Required for kinetochore integrity and the organization of stable microtubule binding sites in the outer plate of the kinetochore (PubMed:15548592). The NDC80 complex synergistically enhances the affinity of the SKA1 complex for microtubules and may allow the NDC80 complex to track depolymerizing microtubules (PubMed:23085020).

Drugs associated with NUF2

Asudemotide

Target

DEPDC1 x IGF2BP3 x KIF20B x LY6K x NUF2

Mechanism

DEPDC1 inhibitors [+4]

Active Org.

OncoTherapy Science, Inc.

Originator Org.

OncoTherapy Science, Inc.

Active Indication

Esophageal Carcinoma [+2]

Inactive Indication-

Drug Highest PhasePhase 3

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

S-588210

Target

IGF2BP3 x LY6K x NUF2

Mechanism

IGF2BP3 agonists [+3]

Active Org.

Shionogi & Co., Ltd. [+1]

Originator Org.

OncoTherapy Science, Inc.

Active Indication

Squamous Cell Carcinoma of Head and Neck [+2]

Inactive Indication

Bladder Cancer [+4]

Drug Highest PhasePhase 2

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Clinical Trials associated with NUF2

NCT04106115

/ RecruitingPhase 1/2IIT

A Phase Ib/II Study to Assess the Safety and Activity of DURvalumab (MEDI4736) in Combination With S-488210/S-488211 vAccine in Non-muscle Invasive Bladder CancEr

DURANCE is a two part, phase Ib/II, multi-centre study to assess the safety and activity of S-488210/S-488211 in combination with durvalumab, in patients with non-muscle invasive bladder cancer (NMIBC).

Start Date25 Mar 2022

Sponsor / Collaborator

University College London

[+2]

NCT04316689

/ CompletedPhase 1

Open-label, Phase 1 Study of S-488210/S-488211 to Evaluate the Safety and Tolerability in Patients With Unresectable Recurrent and/or Metastatic Solid Tumor

The primary objective is to evaluate the safety and tolerability of S-588210 (S-488210+S-488211) in patients with unresectable recurrent and/or metastatic solid tumors.

Start Date30 Jul 2019

Sponsor / Collaborator

Shionogi, Inc.

JPRN-UMIN000023324

/ CompletedPhase 1

Exploratory study to determine S-588410-induced tumor infiltrating lymphocytes and changes in the tumor microenvironment in esophageal cancer patients - Exploratory study to determine S-588410-induced tumor infiltrating lymphocytes and changes in the tumor microenvironment in esophageal cancer patients

Start Date25 Jul 2016

Sponsor / Collaborator

Shionogi & Co., Ltd.

100 Clinical Results associated with NUF2

100 Translational Medicine associated with NUF2

0 Patents (Medical) associated with NUF2

233

Literatures (Medical) associated with NUF2

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·Biochemical Pharmacology

NUF2 activated by YY1 promotes prostate cancer malignancy via p38/MAPK signaling axis and serves as a therapeutic target

Article

Author: Xu, Jing ; Liu, Yongqiang ; Yu, Yang ; Liu, Ji ; Hao, Yajuan ; Ding, Li ; Guo, Hanxu ; Jin, Chengqi ; Zou, Libin ; Luo, Wentao ; Yang, Bin

Prostate cancer (PCa) is one of the most prevalent malignancies in the male urogenital system. Despite extensive research into its mechanisms of initiation and progression, the full scope of its pathophysiology remains insufficiently understood. This study demonstrated that NUF2 was significantly overexpressed in PCa, with its elevated levels correlating with poor patient survival outcomes. Silencing NUF2 notably impaired PCa cell proliferation and metastasis in both in vitro and in vivo models, whereas its overexpression promoted these processes. Additionally, YY1 was identified as a direct transcriptional activator of NUF2, binding to its promoter and enhancing its oncogenic effects through activation of downstream targets. Moreover, NUF2 promoted PCa progression by recruiting p38, accelerating its phosphorylation, and activating the p38/MAPK signaling pathway. Through the PubChem database, fisetin was identified as a small molecule inhibitor of NUF2. Fisetin effectively inhibited PCa cell proliferation, and NUF2 overexpression reversed this inhibitory effect. In conclusion, our results suggest that NUF2 overexpression accelerated PCa progression via the p38/MAPK pathway, regulated by YY1. The identification of fisetin as a NUF2 inhibitor offers a promising therapeutic strategy for targeting NUF2 to impede PCa growth. NUF2 may thus serve as a valuable prognostic biomarker and a potential therapeutic target for PCa.

01 Apr 2025·Journal of Molecular Histology

PBK as a novel biomarker performed excellent diagnostic and prognostic value in HCC associated with immune infiltration and methylation

Article

Author: Lv, Beibei ; Zhang, Xinyi ; He, Na ; Hao, Shuai ; Ye, Na ; Zhang, Fenna ; Wang, Ziyi

Diagnostic and prognosis of hepatocellular carcinoma (HCC) remain major challenge in clinic. This study aimed to explore a gene signature for diagnosis and prognosis prediction of HCC followed by mechanism investigation. Differentially expressed genes (DEGs) in HCC were screened using TCGA. With specific formula, clinic features of prognosis associated DEGs were calculated to obtained a specific model followed by Kaplan-Meier analysis. Protein-protein interaction (PPI) were predicted using STRING and associations between hub gene and clinic features were analyzed using R software. The hub gene was silenced in HCC cell lines followed by cell behaviors analyses. A prognosis associated 14-gene model was identified in this study which could significantly distinguish samples into high-risk and low-risk groups. PBK, BUB1, NUF2, and CDCA8 were the key nodes involved in the 14 gene-coded PPI with high diagnostic values, and only PBK was an independent risk factor of disease specific survival (DSS) of HCC. Moreover, higher PBK was positively correlated with pathological and histological grades, higher AFP, and infiltrations of Th2, T helper cells and aDC of HCC, but negatively correlated with the killer immune cells. Dysregulated methylation might contribute to the higher expression of PBK and silencing PBK significantly suppressed the proliferation, growth, migration, and invasion of HCC cells. PBK, BUB1, NUF2, and CDCA8 played crucial role in prognosis associated 14-gene model with high diagnostic values. Methylation dysregulation-induced PBK accumulation might promote the development of HCC via modulating immune surveillance.

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NUF2

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