Related Experiment Video
Updated: May 4, 2026
Three-Dimensional 3D Tumor Spheroid Invasion Assay
Published on: May 1, 2015
Advances in semaphorin 3B research in tumors (Review)
Xue Zhang1, Ruizeng Feng2, Huanfen Zhao3
1Department of Pathology, The First People's Hospital of Xiantao, Affiliated Hospital of Hubei University of Science and Technology, Xiantao, Hubei 433000, P.R. China.
Abstract:
Advancing precision oncology has driven breakthroughs in understanding oncogenes, tumor suppressors, signaling pathway regulation, apoptosis, and cell cycle control. Molecularly targeted therapies, now integral to malignant tumor treatment, exploit these insights. Functioning as a tumor suppressor, semaphorin 3B (SEMA3B) is frequently inactivated across malignancies via promoter hypermethylation, loss of heterozygosity, and proteolytic cleavage. Its structure-function relies on receptor complex formation, enabling activation of multiple pathways that induce tumor cell apoptosis, arrest the cell cycle, and competitively inhibit vascular endothelial growth factor-binding to neuropilin 1. This blockade of the PI3K/Akt pathway suppresses tumor angiogenesis, metastasis, and proliferation. Therefore, comprehensively elucidating SEMA3B and its interactors is crucial for identifying novel biomarkers for early cancer detection and molecular therapeutic targets. Future research should focus on translating these findings into clinical applications, including the development of SEMA3B-based epigenetic therapies and combination strategies with anti-angiogenic agents. Key challenges remain in fully delineating the context-dependent dual roles of SEMA3B, understanding its complex interactions within the tumor microenvironment, and overcoming its inactivation mechanisms for effective therapeutic restoration.
Insights
Semaphorin 3B (SEMA3B) acts as a tumor suppressor frequently inactivated in cancers. Understanding SEMA3B
Area of Science:
- Oncology
- Molecular Biology
- Cancer Genetics
Background:
- Precision oncology advances understanding of cancer hallmarks like oncogenes, tumor suppressors, and cell cycle control.
- Molecularly targeted therapies are crucial for treating malignant tumors, leveraging insights into cancer biology.
- Semaphorin 3B (SEMA3B) functions as a tumor suppressor, often inactivated in malignancies through epigenetic silencing, genetic alterations, and protein degradation.
Purpose of the Study:
- To comprehensively elucidate the role and interactors of Semaphorin 3B (SEMA3B) in cancer.
- To identify novel biomarkers for early cancer detection based on SEMA3B.
- To explore SEMA3B as a molecular therapeutic target for cancer treatment.
Main Methods:
- Investigating SEMA3B's structure-function relationship and its reliance on receptor complex formation.
- Analyzing SEMA3B's downstream signaling pathways, including apoptosis induction, cell cycle arrest, and inhibition of VEGF signaling.
- Examining the blockade of the PI3K/Akt pathway by SEMA3B and its impact on tumor angiogenesis, metastasis, and proliferation.
Main Results:
- SEMA3B activation of pathways induces tumor cell apoptosis and cell cycle arrest.
- SEMA3B competitively inhibits vascular endothelial growth factor (VEGF) binding to neuropilin 1.
- SEMA3B's blockade of the PI3K/Akt pathway suppresses tumor angiogenesis, metastasis, and proliferation.
Conclusions:
- Elucidating SEMA3B and its interactors is crucial for developing novel cancer biomarkers and therapeutic targets.
- Future research should focus on SEMA3B-based epigenetic therapies and combination strategies with anti-angiogenic agents.
- Challenges include understanding SEMA3B's dual roles, its tumor microenvironment interactions, and overcoming inactivation mechanisms for therapeutic restoration.
