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Non-Canonical Wnt Signaling Pathways

Non-Canonical Wnt Signaling Pathways

Wnt is a zygotic effect gene that is expressed during very early embryonic development. It regulates various processes in animals starting from early development through the adult stage, such as organogenesis in the embryo and maintenance of neuronal and blood stem cells. Wnt proteins can induce a wide variety of intracellular pathways depending upon the specific abilities of different Wnt ligands to form a complex with shared and cognate receptors in the presence of different co-receptors. The...

Non-Canonical Wnt Signaling Pathways

Non-Canonical Wnt Signaling Pathways

Wnt is a zygotic effect gene that is expressed during very early embryonic development. It regulates various processes in animals starting from early development through the adult stage, such as organogenesis in the embryo and maintenance of neuronal and blood stem cells. Wnt proteins can induce a wide variety of intracellular pathways depending upon the specific abilities of different Wnt ligands to form a complex with shared and cognate receptors in the presence of different co-receptors. The...

Canonical Wnt Signaling Pathway

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The gene encoding the main signaling molecules of the Wnt signaling pathways (the Wnt proteins) was discovered almost four decades ago by Nüsslein-Volhard and Wieschaus. They identified and originally named the gene "wingless" (wg) after a phenotype discovered during their landmark genetic screen in Drosophila for body pattern defects. At around the same time, another researcher named Harold Varmus found that a murine tumor virus activates the mammalian wg homolog, Int-1, which results in tumor...

Canonical Wnt Signaling Pathway

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The gene encoding the main signaling molecules of the Wnt signaling pathways (the Wnt proteins) was discovered almost four decades ago by Nüsslein-Volhard and Wieschaus. They identified and originally named the gene "wingless" (wg) after a phenotype discovered during their landmark genetic screen in Drosophila for body pattern defects. At around the same time, another researcher named Harold Varmus found that a murine tumor virus activates the mammalian wg homolog, Int-1, which results in tumor...

Targeted Cancer Therapies

Targeted Cancer Therapies

The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against specific...

Targeted Cancer Therapies

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The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against specific...

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A Syngeneic Orthotopic Osteosarcoma Sprague Dawley Rat Model with Amputation to Control Metastasis Rate

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Targeting the Wnt pathway in synovial sarcoma models.

Whitney Barham¹, Andrea L Frump, Taylor P Sherrill

¹1Department of Cancer Biology, 2Division of Hepatobiliary Surgery, Department of Surgery, 3Division of Allergy, Pulmonary and Critical Care Medicine, Department of Medicine, and 4Vanderbilt Ingram Cancer Center, Vanderbilt University Medical Center; 5Department of Cell and Developmental Biology, Vanderbilt University; 6StemSynergy Therapeutics, Inc., Nashville, Tennessee; 7Department of Pediatrics-Nutrition, Baylor College of Medicine, Houston, Texas; and 8Department of Human Genetics, Howard Hughes Medical Institute, University of Utah, Salt Lake City, Utah.

Cancer Discovery

|August 8, 2013

Summary

Aberrant Wnt/β-catenin signaling, driven by the SYT-SSX oncogene, fuels synovial sarcoma. Inhibiting this pathway through genetic or pharmacological means halts tumor growth, offering new therapeutic strategies for this aggressive cancer.

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A Mouse Model of Incompletely Resected Soft Tissue Sarcoma for Testing (Neo)adjuvant Therapies

A Mouse Model of Incompletely Resected Soft Tissue Sarcoma for Testing (Neo)adjuvant Therapies

Published on: July 28, 2020

Area of Science:

Oncology
Molecular Biology
Cancer Genetics

Background:

Synovial sarcoma is a rare, aggressive soft-tissue cancer predominantly affecting children and young adults.
Current systemic therapies for synovial sarcoma are largely ineffective.
The oncogenic driver SYT-SSX (SS18-SSX) is crucial for sarcoma development, but its precise mechanism of action is unclear.

Purpose of the Study:

To elucidate the role of the SYT-SSX oncogene in synovial sarcoma pathogenesis.
To investigate the involvement of Wnt/β-catenin signaling in SYT-SSX-driven oncogenesis.
To explore therapeutic strategies targeting the Wnt pathway in synovial sarcoma.

Main Methods:

Utilized an SYT-SSX2 transgenic mouse model to study sarcoma initiation.
Employed cell-based assays and synovial sarcoma xenograft models.
Investigated Wnt signaling inhibition via genetic deletion of β-catenin, coreceptor blockade, and small-molecule CK1α activators.

Main Results:

Demonstrated that SYT-SSX2 aberrantly activates constitutive Wnt/β-catenin signaling.
Showed that genetic loss of β-catenin prevents synovial sarcoma formation.
Confirmed that inhibiting the Wnt cascade arrests tumor growth in preclinical models.
Correlated SYT-SSX2-induced Wnt/β-catenin upregulation with nuclear reprogramming functions.

Conclusions:

The Wnt/β-catenin signaling pathway plays a pivotal role in SYT-SSX2-induced synovial sarcoma development.
Targeting the Wnt/β-catenin cascade presents a promising therapeutic avenue for synovial sarcoma.
These findings open new possibilities for developing effective curative agents for this challenging malignancy.