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Last update 08 May 2025

TPX2

Last update 08 May 2025

Basic Info

Synonyms

C20orf1, C20orf2, Differentially expressed in cancerous and non-cancerous lung cells 2

+ [12]

Introduction

Spindle assembly factor required for normal assembly of mitotic spindles. Required for normal assembly of microtubules during apoptosis. Required for chromatin and/or kinetochore dependent microtubule nucleation. Mediates AURKA localization to spindle microtubules (PubMed:18663142, PubMed:19208764, PubMed:37728657). Activates AURKA by promoting its autophosphorylation at 'Thr-288' and protects this residue against dephosphorylation (PubMed:18663142, PubMed:19208764). TPX2 is inactivated upon binding to importin-alpha (PubMed:26165940). At the onset of mitosis, GOLGA2 interacts with importin-alpha, liberating TPX2 from importin-alpha, allowing TPX2 to activate AURKA kinase and stimulate local microtubule nucleation (PubMed:26165940).

Drugs associated with TPX2

US20240101538

Patent Mining

Target

Aurora A x TPX2 x c-Myc

Mechanism

Aurora A modulators

Active Org.

Eberhard Karls Universität Tübingen

Originator Org.

Eberhard Karls Universität Tübingen

Active Indication

Dermatophilosis [+2]

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with TPX2

100 Translational Medicine associated with TPX2

0 Patents (Medical) associated with TPX2

719

Literatures (Medical) associated with TPX2

01 Jun 2025·Computers in Biology and Medicine

FDA-approved Levophed as an alternative multitargeted therapeutic against cervical cancer transferase, cell cycle, and regulatory proteins

Article

Author: Gupta, Dinesh ; Bano, Nagmi ; Ahmad, Shaban ; Raza, Khalid

Despite the availability of Pap tests and HPV vaccines, Cervical Cancer continues to be a significant factor contributing to women's deaths. It poses severe consequences to women's health. The disease's severity lies in its potential to progress silently in its early stages, mainly detected in its advanced stage, and clinical treatment is challenging due to drug resistance. This study aims to identify multitargeted lead molecules based on the interactome of Cervical Cancer-related crucial genes, which can help develop drug-resistant therapies. We have considered 9 crucial Cervical Cancer genes, namely BUBR1, CCNB1, FEN1, MAD2, MCM10, MCM6, ITGB8, POLE, and TPX2, to perform gene network analysis and Gene Ontology enrichment studies to identify the potential hub genes and their role. Further, we performed multitarget screening using multisampling algorithms HTVS, SP, and XP to screen the protein products of the 9 genes for their binding affinity for the FDA-approved drugs library. The binding affinities of the compounds were evaluated using MM\GBSA that identified multitargeted potential inhibitor as a Levophed for Cervical Cancer, and the docking results showed a range of MM/GBSA scores, varying from -8.35 to -5.38 kcal/mol for docking, and -43.41 to -19.37 kcal/mol for MM/GBSA scoring. The protein residues that interact the most with Levophed are ALA, THR, ILE, ASN, GLY, ASP, LEU, LYS, VAL, GLN, PRO, CYS, GLU, and TYR. The pharmacokinetic properties and WaterMap computations also support the idea that the compound can potentially become a drug candidate. Furthermore, all 9 complexes were simulated for 100ns, resulting in cumulative deviation and fluctuation of <2 Å, with many intermolecular interactions and binding free energy computations supporting the studies. The study shows that Levophed could treat Cervical Cancer without encountering drug resistance- however, experimental studies are needed to confirm the accuracy.

01 Jun 2025·Current Medicinal Chemistry

Clinical Significance of a Novel Vasculogenic Mimicry-based Prognostic Model in Hepatocellular Carcinoma

Article

Author: Zeng, Yifan ; Jiang, Shuwen ; Ruan, Bing ; Pan, Liya ; Chen, Lin ; Lou, Zhuoqi ; Shi, Qingmiao ; Zhang, Yongtao

Background:Vasculogenic mimicry, a novel neovascularization pattern of aggressive tumors, is associated with poor clinical outcomes.Objective:The aim of this research was to establish a new model, termed VC score, to predict the prognosis, Tumor Microenvironment (TME) components, and immunotherapeutic response in Hepatocellular Carcinoma (HCC).Methods:The expression data of the public databases were used to develop the prognostic model. Consensus clustering was performed to confirm the molecular subtypes with ideal clustering efficacy. The high- and low-risk groups were stratified utilizing the VC score. Various methodologies, including survival analysis, single-sample Gene Set Enrichment Analysis (ssGSEA), Tumor Immune Dysfunction and Exclusion scores (TIDE), Immunophenoscore (IPS), and nomogram, were utilized for verification of the model performance and to characterize the immune status of HCC tissues. GSEA was performed to mine functional pathway information.Results:The survival and immune characteristics varied between the three molecular subtypes. A five-gene signature (TPX2, CDC20, CFHR4, SPP1, and NQO1) was verified to function as an independent predictive factor for the prognosis of patients with HCC. The high-risk group exhibited lower Overall Survival (OS) rates and higher mortality rates in comparison to the low-risk group. Patients in the low-risk group were predicted to benefit from immune checkpoint inhibitor therapy and exhibit increased sensitivity to immunotherapy. Enrichment analysis revealed that signaling pathways linked to the cell cycle and DNA replication processes exhibited enrichment in the high-risk group.Conclusions:The VC score holds the potential to establish individualized treatment plans and clinical management strategies for patients with HCC.

01 Jun 2025·Life Science Alliance

TPX2 lactylation is required for the cell cycle regulation and hepatocellular carcinoma progression

Article

Author: Gao, Ping ; Zhang, Junjiao ; Liu, Shengzhi ; Zhang, Yi ; Qian, Xiaoyu ; Meng, Xiang ; Wang, Mingjie ; Zhong, Xiuying ; Cai, Jin

Targeting protein for Xklp2 (TPX2) is critical for mitosis and spindle assembly because of its control of Aurora kinase A (AURKA). However, the regulation of TPX2 activity and its subsequent effects on mitosis and cancer progression remain unclear. Here, we show that TPX2 is lactylated at K249 in hepatocellular carcinoma (HCC) tumour tissues and that this process is regulated by the lactylase CBP and the delactylase HDAC1. Lactate reduction via either shRNAs targeting lactate dehydrogenase A or the lactate dehydrogenase A inhibitor GSK2837808A decreases the level of TPX2 lactylation. Importantly, TPX2 lactylation is required for the cell cycle regulation and tumour growth. Mechanistically, TPX2 lactylation disrupts protein phosphatase 1 (PP1) binding to AURKA, enhances AURKA T288 phosphorylation, and facilitates the cell cycle progression. Overall, our study reveals a previously unappreciated role of TPX2 lactylation in regulating cell cycle progression and HCC tumorigenesis, exposing an important correlation between metabolic reprogramming and cell cycle regulation in HCC.

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TPX2

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