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Last update 08 May 2025

CELSR3

Last update 08 May 2025

Basic Info

Synonyms

ADGRC3, adhesion G protein-coupled receptor C3, Cadherin EGF LAG seven-pass G-type receptor 3

+ [16]

Introduction

Receptor that may have an important role in cell/cell signaling during nervous system formation.

Drugs associated with CELSR3

HG-1025

Target

CELSR3 x Multiple EGF like domain

Mechanism

CELSR3 modulators [+1]

Active Org.-

Originator Org.

Human Genome Sciences, Inc.

Active Indication-

Inactive Indication

Neoplasms

Drug Highest PhasePending

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with CELSR3

100 Translational Medicine associated with CELSR3

0 Patents (Medical) associated with CELSR3

135

Literatures (Medical) associated with CELSR3

01 Apr 2025·Human Genetics

Conventional and genetic association between migraine and stroke with druggable genome-wide Mendelian randomization

Article

Author: Mao, Minzi ; Song, Yao ; Zhang, Yuyang ; Wang, Xiaoyu ; Rao, Yufang ; Li, Junhong ; Hu, Xin ; Zhao, Yu ; Feng, Lan ; Luo, Yaxin ; Ren, Jianjun ; Pang, Wendu ; Qiu, Ke ; Shu, Tao

The genetic relationship between migraine and stroke remains underexplored, particularly in the context of druggable targets. Previous studies have been limited by small sample sizes and a lack of focus on genetic-targeted therapies for these conditions. We analyzed the association and causality between migraine and stroke using multivariable logistic regression in the UK Biobank cohort and Mendelian randomization (MR) analyses based on genome-wide association study (GWAS) data. Integrating expression quantitative trait loci (eQTLs) data from blood and brain regions, we explored the phenotypic and genetic links between migraine medications, drug target, and stroke. Additionally, we explored novel druggable genes for migraine and evaluated their effects on migraine signaling molecules and stroke risk. Migraine was significantly associated with stroke, particularly ischemic stroke (IS) and intracerebral hemorrhage (ICH), with MR analysis confirming a causal link to ICH. HTR1A emerged as a potential link between antidepressants (preventive medications for migraine) and stroke. We identified 17 migraine-related druggable genes, with 5 genes (HMGCR, TGFB1, TGFB3, KCNK5, IMPDH2) associated with nine existing drugs. Further MR analysis identified correlation of CELSR3 and IMPDH2 with cGMP pathway marker PRKG1, and identified KCNK5, PLXNB1, and MDK as novel migraine-associated druggable genes significantly linked to the stroke risks. These findings established the phenotypic and genetic link between migraine, its medication and stroke, identifying potential targets for single and dual-purpose therapies for migraine and stoke, and emphasized the need for further research to validate these associations.

11 Feb 2025·Proceedings of the National Academy of Sciences

Extrinsic induction of apoptosis and tumor suppression via the p53–Reprimo–Hippo–YAP/TAZ–p73 pathway

Article

Author: Sadaie, Mahito ; Nakano, Airi ; Kaneda, Atsushi ; Okabe, Atsushi ; Tajima, Tomoko ; Ishikawa, Fuyuki ; Araki, Kimi ; Krishnaraj, Jayaraman ; Tabata, Yuko ; Sada, Akane ; Ohki, Rieko ; Sakaguchi, Yukiko ; Takikawa, Masahiro ; Mochizuki, Ami ; Matsushita, Shu ; Wakabayashi, Yuichi ; Fujiki, Ryoji ; Watanabe, Yuzo

Tumor progression is suppressed by inherent cellular mechanisms such as apoptosis. The p53 tumor suppressor gene is the most commonly mutated gene in human cancer and plays a pivotal role in tumor suppression. RPRM is a target gene of p53 known to be involved in tumor suppression, but its molecular function has remained elusive. Here, we report that Reprimo (the protein product of RPRM ) is secreted and extrinsically induces apoptosis in recipient cells. We identified FAT1, FAT4, CELSR1, CELSR2, and CELSR3, members of the protocadherin family, as receptors for Reprimo. Subsequent analyses revealed that Reprimo acts upstream of the Hippo–YAP/TAZ–p73 axis and induces apoptosis by transactivating various proapoptotic genes. In vivo analyses further support the tumor-suppressive effects of secreted Reprimo. These findings identify the p53–Reprimo–Hippo–YAP/TAZ–p73 axis as an extrinsic apoptosis pathway that plays a crucial role in tumor suppression. Our finding of the innate tumor eliminator Reprimo and the downstream pathway offers a promising avenue for the pharmacological treatment of cancer.

01 Feb 2025·Cancer Research Communications

Expression Patterns of DLL3 across Neuroendocrine and Non-neuroendocrine Neoplasms Reveal Broad Opportunities for Therapeutic Targeting

Article

Author: Storey, Kathleen M. ; Soares, Heloisa P. ; Elliott, Andrew ; Cichocki, Frank ; Lozada, John R. ; Zorko, Nicholas A. ; Beltran, Himisha ; Kumar, Akhilesh ; Carneiro, Benedito A. ; Wacker, James ; Egusa, Emily A. ; Miller, Jeffrey S. ; Ryan, Charles J. ; Lou, Emil ; Heath, Elisabeth I. ; Hwang, Justin H. ; Crymes, Anthony ; Evans, Mark G. ; Antonarakis, Emmanuel S.

AbstractNeuroendocrine neoplasms (NEN) encompass a diverse set of malignancies with limited precision therapy options. Recently, therapies targeting DLL3 have shown clinical efficacy in aggressive NENs, including small cell lung cancers and neuroendocrine prostate cancers. Given the continued development and expansion of DLL3-targeted therapies, we sought to characterize the expression of DLL3 and identify its clinical and molecular correlates across diverse neuroendocrine and non-neuroendocrine cancers. Here, we interrogated paired DNA and RNA-sequencing from 1,589 NENs across 29 sites, as well as 203,252 tumors across 47 cancer types. We found that high transcriptomic levels of DLL3 correlated with more aggressive histologic and mutational patterns in NENs, with adverse survival outcomes being reflected in NENs originating from the lung, pancreas, stomach, and small bowel. The heterogeneity in DLL3 expression across NENs was largely explained by site of origin, with lung, prostate, and bladder NENs exhibiting relatively high levels of DLL3, whereas gastroenteropancreatic NENs displayed relatively low expression levels. Although the therapeutic targeting of DLL3 may be less applicable for gastroenteropancreatic NENs, we did find an upregulation of alternative targets such as SEZ6, CELSR3, and SSTR2 in these settings. Lastly, expanding our investigation into non-neuroendocrine cancers, we detected an enrichment of DLL3 in both low-grade and high-grade gliomas, Merkel cell carcinomas, medulloblastomas, and melanomas, with such enrichment being associated with prolonged overall survival in gliomas, but worse overall survival in melanomas. Altogether, we demonstrate that DLL3 represents an attractive target for subsets of neuroendocrine and non-neuroendocrine cancers and uncover opportunities for future therapeutic strategies.Significance:DLL3-targeted therapies have recently shown robust clinical efficacy in aggressive neuroendocrine cancers, positioning them to fulfill a great unmet need in these settings. Here, we examine the clinical and biological correlates of DLL3 expression in both neuroendocrine and non-neuroendocrine cancers. Our findings may stimulate the development and application of DLL3-targeted therapies, as well as other precision therapies, in neuroendocrine cancers and beyond.

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CELSR3

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