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Last update 08 May 2025

OSR1

Last update 08 May 2025

Basic Info

Synonyms

ODD, odd-skipped related transcription factor 1, OSR1

+ [1]

Introduction

Transcription factor that plays a role in the regulation of embryonic heart and urogenital development.

Drugs associated with OSR1

closantel

Target

OSR1 x STK39

Mechanism

OSR1 inhibitors [+1]

Active Org.

University of Birmingham

Originator Org.

University of Birmingham

Active Indication

Hypertension

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Rafoxanide

Target

OSR1 x STK39

Mechanism

OSR1 inhibitors [+1]

Active Org.

University of Birmingham

Originator Org.

University of Birmingham

Active Indication

Hypertension

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with OSR1

100 Translational Medicine associated with OSR1

0 Patents (Medical) associated with OSR1

395

Literatures (Medical) associated with OSR1

31 Dec 2025·Animal Cells and Systems

Asxl1 loss in mice leads to microcephaly by regulating neural stem cell survival

Article

Author: Byun, Sukyoung ; Um, Soo-Jong ; Kim, Hyeju ; Kim, A.-Reum

Additional sex comb-like 1 (ASXL1) is a chromatin-associated factor essential for transcriptional regulation. De novo truncating mutations in the ASXL1 gene are linked to Bohring-Opitz syndrome, a developmental disorder characterized by microcephaly; however, the role of Asxl1 in brain development remains unclear. In this study, we demonstrate that Asxl1 deletion in mice induces microcephaly, primarily caused by a reduction in the size and number of cortical neurons. Asxl1 ablation disrupts neural stem cell (NSC) maintenance, as evidenced by decreased proliferation and increased apoptosis. Transcriptomic analysis of Asxl1-deficient NSCs revealed 4,635 differentially expressed genes, including 2,262 upregulated and 2,373 downregulated genes. Gene ontology analysis indicated that Asxl1 regulates NSC survival through the histone methyltransferase Ezh2, a core component of the Polycomb Repressive Complex 2 (PRC2). Inhibition of H3K27me3 using GSK343 significantly reduced the viability of wild-type NSCs, but had a markedly diminished effect on Asxl1-deficient NSCs. Furthermore, Ezh2 target genes associated with apoptosis, such as Epha7 and Osr1, were upregulated in wild-type NSCs following GSK343 treatment but not significantly affected in Asxl1-deficient NSCs. These findings establish Asxl1 as a critical regulator of NSC survival and neurogenesis via Ezh2-mediated chromatin modification and provide insights into the mechanisms underlying microcephaly in developmental disorders.

14 Mar 2025·ACS Pharmacology & Translational Science

Oxidative Stress-Responsive 1 Kinase Catalytic Activity Promotes Triple Negative Breast Cancer Oncogenic Potential

Article

Author: Banerjee, Sourav ; Sharma, Ira ; Jones, Samuel ; Mehellou, Youcef ; Waters, Loren ; Fdel, Azeza M. ; Atack, John R. ; Gee, Julia

The protein kinase OSR1 has been highlighted as a biomarker for a poor prognosis in breast cancer (BC) patients. To further decipher the mechanism underpinning this, we studied the expression, phosphorylation status, and catalytic activity of OSR1 across a series of BC cell lines. OSR1 was found to be expressed across the various luminal and triple negative BC (TNBC) cell lines studied, although it was only constitutively active in the highly migratory TNBC cell line MDA-MB-231. Although this cell line carries p53 mutations, our data indicated that OSR1 constitutive kinase activity of the OSR1 in MDA-MB-231 was independent of p53. Interestingly, the inhibition of OSR1 had no significant impact on MDA-MB-231 cell viability, but it was found to contribute to its substantial cell migration and invasion, as this was significantly attenuated by the WNK/OSR1 inhibitor WNK463. Analogously, the overexpression of constitutively active OSR1 in the poorly migrating BC cell line MCF7 enhanced its cell mobility. Collectively, our results indicate that the pharmacological inhibition of OSR1 could be a promising novel strategy for preventing the oncogenic potential of TNBC.

01 Mar 2025·Oral Diseases

OSR1 suppresses oral squamous cell carcinoma proliferation and migration via the AXIN2/β‐catenin pathway

Article

Author: Guo, Xintong ; Gao, Jing ; Zhao, Gaoye ; Liu, Chongshen ; Du, Xinyi ; Dong, Wei ; Huang, Zunzhi

AbstractObjectivesThe odd‐skipped related transcription factor 1 (OSR1) gene exerts distinct regulatory effects on tumorigenesis and development in various cancer types. However, the precise role of OSR1 in oral squamous cell carcinoma (OSCC) remains to be elucidated.MethodsGEPIA 2 and TCGA databases were utilized to analyze the OSR1 expression in head and neck squamous cell carcinoma (HNSC) patients and its impact on prognosis. Hematoxylin–eosin staining, immunohistochemistry, immunofluorescence, western blotting, and RT‐qPCR were employed to detect the OSR1 expression in OSCC tissues and cells. Lentivirus transfection was utilized for overexpression and downexpression of OSR1 in OSCC. CCK8 cell proliferation assay, colony formation and cell scratch assay were conducted to investigate the effects of OSR1 on biological behavior of OSCC cells. Western blotting and RT‐qPCR were applied to investigate the regulatory mechanism of OSR1 on AXIN2/β‐catenin signaling pathway.ResultsOSR1 expression was significantly decreased in HNSC patients, OSCC tissues and cells, leading to a decrease in 5‐year survival rate. OSR1 overexpression inhibited the proliferation and migration of OSCC cells, and the AXIN2/β‐catenin signaling pathway was inhibited. Silencing OSR1 had the opposite effect.ConclusionsOSR1 functioned as a tumor suppressor gene in OSCC proliferation and migration by regulating the AXIN2/β‐catenin signaling pathway.

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OSR1

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