Related Experiment Video
Updated: Aug 1, 2025

Modeling Paracrine Noncanonical Wnt Signaling In Vitro
Published on: December 10, 2021
The role of Wnt, ARL4C, and Sema3A in developmental process and disease pathogenesis
Shinsuke Fujii1,2, Tamotsu Kiyoshima1
1Laboratory of Oral Pathology, Division of Maxillofacial Diagnostic and Surgical Sciences, Faculty of Dental Science, Kyushu University, Fukuoka, Japan.
Abstract:
Various types of tumors, including malignant and benign ones, occur in the oral cavity. These arise from the mucosal epithelium, odontogenic epithelium, and salivary gland. To date, few major driver events in oral tumors have been identified. Accordingly, molecular targets in anti-tumor therapy for oral tumors are lacking. We focused on elucidating the function of aberrantly activated signal transduction related to oral tumor formation, especially in oral squamous cell carcinoma, ameloblastoma, and adenoid cystic carcinoma, which are raised as common oral tumors. Wnt/β-catenin-dependent pathway is involved in the developmental process, organ homeostasis and disease pathogenesis through regulating various cellular functions by enhancing transcriptional activity. Recently, we identified ADP-ribosylation factor (ARF)-like 4c (ARL4C) and Semaphorin 3A (Sema3A), the expression of which is regulated by Wnt/β-catenin-dependent pathway, and characterized their functions in the developmental process and tumor formation. This review highlights the recent advances in understanding the roles of Wnt/β-catenin-dependent pathway, ARL4C and Sema3A, as determined by pathological and experimental studies.
Insights
This study explores the Wnt/β-catenin pathway
Area of Science:
- Oncology
- Molecular Biology
- Cell Signaling
Background:
- Oral tumors, including squamous cell carcinoma, ameloblastoma, and adenoid cystic carcinoma, lack identified major driver events and molecular targets for therapy.
- Aberrant signal transduction pathways are implicated in oral tumor formation, necessitating further investigation into their roles.
- The Wnt/β-catenin-dependent pathway is crucial for development, homeostasis, and pathogenesis, regulating cellular functions via transcriptional activity.
Purpose of the Study:
- To elucidate the function of aberrantly activated signal transduction pathways in oral tumorigenesis.
- To investigate the roles of ADP-ribosylation factor (ARF)-like 4c (ARL4C) and Semaphorin 3A (Sema3A) in oral tumor development.
- To highlight recent advances in understanding the Wnt/β-catenin pathway, ARL4C, and Sema3A in oral tumors.
Main Methods:
- Pathological studies of oral tumors.
- Experimental characterization of gene and protein functions.
- Review of recent scientific literature on Wnt/β-catenin signaling, ARL4C, and Sema3A.
Main Results:
- The Wnt/β-catenin-dependent pathway regulates the expression of ARL4C and Sema3A.
- ARL4C and Sema3A play significant roles in developmental processes and tumor formation.
- Aberrant activation of this pathway contributes to the pathogenesis of common oral tumors.
Conclusions:
- The Wnt/β-catenin pathway, ARL4C, and Sema3A are critical in oral tumor development and present potential therapeutic targets.
- Understanding these molecular mechanisms is essential for advancing anti-tumor therapies for oral cancers.
- Further research into these pathways may lead to novel diagnostic and therapeutic strategies for oral malignancies.
More Related Videos
Related Concept Videos
Canonical Wnt Signaling Pathway
Non-Canonical Wnt Signaling Pathways
Notch Signaling Pathway
The Notch gene came into the limelight in 1914 after the discovery that its mutation in Drosophila melanogaster leads to a serrated (or "notched") wing margin phenotype. It was not...
Role Of Notch Signalling In Intestinal Stem Cell Renewal
Direct cell-to-cell contact is needed for the activation of Notch signaling. The signal is initiated when a notch ligand binds to a receptor on an adjacent cell, also...
Cadherins in Tissue Organization
Cell Sorting During Development
Cell sorting plays an...
Hedgehog Signaling Pathway

