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Last update 08 May 2025

ROBO1

Last update 08 May 2025

Basic Info

Synonyms

Deleted in U twenty twenty, DUTT1, FLJ21882

+ [7]

Introduction

Receptor for SLIT1 and SLIT2 that mediates cellular responses to molecular guidance cues in cellular migration, including axonal navigation at the ventral midline of the neural tube and projection of axons to different regions during neuronal development (PubMed:10102268, PubMed:24560577). Interaction with the intracellular domain of FLRT3 mediates axon attraction towards cells expressing NTN1 (PubMed:24560577). In axon growth cones, the silencing of the attractive effect of NTN1 by SLIT2 may require the formation of a ROBO1-DCC complex (By similarity). Plays a role in the regulation of cell migration via its interaction with MYO9B; inhibits MYO9B-mediated stimulation of RHOA GTPase activity, and thereby leads to increased levels of active, GTP-bound RHOA (PubMed:26529257). May be required for lung development (By similarity).

Drugs associated with ROBO1

ASC-101 (Ascle)

Target

ROBO1

Mechanism

ROBO1 inhibitors

Active Org.

Ascle Therapeutics (Suzhou) Co., Ltd.

Originator Org.

Ascle Therapeutics (Suzhou) Co., Ltd.

Active Indication

Breast Cancer

Inactive Indication-

Drug Highest PhaseIND Application

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

ASC-103

Target

ROBO1

Mechanism

ROBO1 inhibitors

Active Org.

Ascle Therapeutics (Suzhou) Co., Ltd.

Originator Org.

Ascle Therapeutics (Suzhou) Co., Ltd.

Active Indication

Lung Cancer

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Anti-ROBO1 CAR T cells(National Research Council Canada)

Target

ROBO1

Mechanism

ROBO1 inhibitors

Active Org.

McMaster University [+1]

Originator Org.

National Research Council of Canada [+1]

Active Indication

Glioblastoma

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Clinical Trials associated with ROBO1

NCT03931720

/ Unknown statusPhase 1/2

Clinical Research of ROBO1 Specific BiCAR-NK/T Cells on Patients With Malignant Tumor

Immunotherapy has become the major breakthrough and the most promising treatment, with the host of development of tumor biology, molecular biology and immunology. ROBO1 is a potential target and spectacular paradigm in the diagnosis and treatment of solid tumors. This study is for evaluation of the safety and efficacy of ROBO1 CAR-NK/T cell immunotherapy for malignant tumors.

Start Date01 May 2019

Sponsor / Collaborator

Ascle Therapeutics (Suzhou) Co., Ltd.

100 Clinical Results associated with ROBO1

100 Translational Medicine associated with ROBO1

0 Patents (Medical) associated with ROBO1

721

Literatures (Medical) associated with ROBO1

01 Jul 2025·Metabolism

Mechanical activation of adipose tissue macrophages mediated by Piezo1 protects against diet-induced obesity by regulating sympathetic activity

Article

Author: Wang, Shuwen ; Li, Xin ; Sheng, Zi ; Hu, Xiang ; Zhang, Xiaoyu ; Liu, Xinyue ; Peng, Jun ; Jiang, Nan ; Leng, Shaoqiu ; Zhao, Ruxia ; Feng, Qi

OBJECTIVEObesity-induced mechanical changes in white adipose tissue (WAT), including adipocyte hypertrophy and fibrosis, are hypothesized to alter adipose tissue macrophage (ATM) function through mechanosensitive pathways. This study aimed to determine whether the mechanosensor Piezo1 in ATMs regulates obesity-associated metabolic dysfunction and thermogenesis.METHODSTo investigate macrophage Piezo1 in obesity, myeloid-specific Piezo1-deficient mice (Piezo1^∆lyz2) and littermate controls (Piezo1^flox/+) were fed a high-fat diet (HFD) to induce obesity for 12 weeks. Metabolic assessments (GTT/ITT), tissue analyses (H&E staining, micro-CT), and RNA-seq were performed. Bone marrow transplantation and co-culture experiments (BMDMs with 3T3L1 adipocytes/PC12 neurons) were performed to evaluate macrophage-adipocyte/neuron crosstalk. Sympathetic activity was tested via cold exposure, NE measurement, and 6-OHDA/αMPT denervation. Molecular mechanisms were investigated using ChIP-qPCR.RESULTSPiezo1^∆lyz2 mice exhibited aggravated HFD-induced obesity and insulin resistance despite reduced pro-inflammatory responses. Piezo1 deficiency in ATMs suppressed Slit3-ROBO1 signaling, leading to diminished NE secretion and impaired thermogenesis. Pharmacological inhibition of NE release (6-OHDA) or ROBO1 knockdown (shROBO1) abolished thermogenic disparities between Piezo1^∆lyz2 and control mice. Mechanistically, Piezo1 activation triggered SP1 nuclear translocation, directly binding to the Slit3 promoter to drive Slit3 transcription and secretion.CONCLUSIONPiezo1 in ATMs mitigates obesity progression by promoting Slit3-ROBO1-dependent NE secretion and thermogenesis, independent of its pro-inflammatory role. This mechanosensitive pathway links WAT mechanical remodeling to metabolic regulation, which may offer a novel approach for managing obesity.

01 Apr 2025·Molecular Biology of the Cell

MYC regulation of the miR-92-Robo1 axis in Slit-mediated commissural axon guidance

Article

Author: Khot, Bhakti ; Nathan, Anagaa ; Majumder, Tanushree ; Liu, Guofa ; Suriyaarachchi, Harindi

In the developing spinal cord, translational repression of Robo1 expression by microRNA-92 (miR-92) in precrossing commissural axons (CAs) inhibits Slit/Robo1-mediated repulsion facilitating commissural axon projection and midline crossing; however, the regulatory mechanisms governing miR-92 expression in the developing commissural neurons are currently lacking. Here, we propose that the transcription factor MYC regulates miR-92 expression in the developing spinal cord (of either sex) to control Robo1 levels in precrossing CAs, modulating Slit/Robo1-mediated repulsion and midline crossing. MYC, miR-92, and Robo1 are differentially expressed in the developing chicken spinal cord. MYC binds to the promoter region upstream of the gga-miR-92 gene in vitro. MYC knockdown dramatically decreases miR-92 expression and increases chicken Robo1 (cRobo1) levels. In contrast, overexpression of MYC significantly induces miR-92 expression and reduces cRobo1 levels. MYC knockdown or overexpression results in significant inhibition or induction of miR-92 activity in the developing chicken spinal cord, respectively. Disruption of the MYC-dependent regulation of the miR-92-cRobo1 axis affects Slit2-mediated CA growth cone collapse in vitro and impairs CA projection and midline crossing in vivo. These results elucidate the role of the MYC-miR-92-cRobo1 axis in Slit2/Robo1-mediated CA repulsion and midline crossing.

01 Mar 2025·Neoplasia

Identification of 68 HLA-A24 and -A2-restricted cytotoxic T lymphocyte-inducing peptides derived from 10 common cancer-specific antigens frequently expressed in various solid cancers

Article

Author: Ohnuki, Kazunobu ; Tsukamoto, Nobuo ; Takenouchi, Kazumasa ; Nakatsura, Tetsuya ; Suzuki, Toshihiro ; Kinoshita, Hiroki

Targeting cancer antigens expressed in cancer cells is necessary to develop cancer-specific immunotherapy. We have performed immunohistochemical analysis of various solid cancer specimens, adding ROBO1, AFP, TGFBI, EphB4, CLDN1, and LAT1 to the previously studied glypican-3 (GPC3), HSP105α, FOXM1, and SPARC, and found that these 10 common cancer antigens are sufficient to cover most solid cancers. These antigens were frequently expressed in various solid cancers but shown to be rarely ex-pressed, with some exceptions, in non-cancerous normal organs adjacent to the cancer. In this study, we predicted 72 and 73 peptides that bind to HLA-A24 and -A2 in silico from the full-length amino acid sequences of these 10 common cancer antigens and immunized each HLA transgenic mouse with a cocktail of synthesized peptides together with the poly I:CLC three times weekly to analyze the antigen-specific immune response. As a result, 68 peptide sequences (30 and 38, respectively) were identified that had higher cytotoxic T lymphocyte (CTL) induction ability than GPC3 298-306 and GPC3 144-152 used in the clinical trials. Furthermore, experiments with cocktail peptide vaccines using mouse models expressing subcutaneous tumors of each antigen showed promising results in terms of safety and efficacy. These peptides identified in this study, derived from 10 common cancer antigens covering all solid cancers, are expected to be clinically applicable as cocktail peptide vaccines.

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ROBO1

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