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Updated: May 16, 2026
Development and Maintenance of a Preclinical Patient Derived Tumor Xenograft Model for the Investigation of Novel Anti-Cancer Therapies
Published on: September 30, 2016
Targeting MCT-1 oncogene inhibits Shc pathway and xenograft tumorigenicity
Hung-Ju Shih1, Hsiao-Huei Chen, Yen-An Chen
1Institute of Molecular and Genomic Medicine, National Health Research Institutes, Taiwan.
Abstract:
Overexpression of Shc adaptor proteins is associated with mitogenesis, carcinogenesis and metastasis. Multiple copies in T-cell malignancy 1 (MCT-1) oncoprotein promotes cell proliferation, survival and tumorigenic effects. Our current data show that MCT-1 is a novel regulator of Shc-Ras-MEK-ERK signaling and MCT-1 is significantly co-activated with Shc gene in human carcinomas. The knockdown of MCT-1 enhances apoptotic cell death accompanied with the activation of caspases and cleavage of caspase substrates under environmental stress. The cancer cell proliferation, chemo-resistance and tumorigenic capacity are proved to be effectively suppressed by targeting MCT-1. Accordingly, an important linkage between MCT-1 oncogenicity and Shc pathway in tumor development has now been established. Promoting MCT-1 expression by gene hyperactivation may be recognized as a tumor marker and MCT-1 may serve as a molecular target of cancer therapy.
Insights
The T-cell malignancy 1 (MCT-1) oncoprotein drives cancer by regulating Shc-Ras-MEK-ERK signaling. Targeting MCT-1 suppresses cancer cell proliferation and chemo-resistance, establishing it as a potential tumor marker and therapeutic target.
Area of Science:
- Oncology
- Molecular Biology
- Signal Transduction
Background:
- Shc adaptor proteins are implicated in cancer development, including cell proliferation, carcinogenesis, and metastasis.
- The T-cell malignancy 1 (MCT-1) oncoprotein has been shown to promote cell survival and tumorigenic effects.
Purpose of the Study:
- To investigate the role of MCT-1 as a novel regulator of Shc-Ras-MEK-ERK signaling.
- To establish the link between MCT-1 oncogenicity and the Shc pathway in human carcinomas.
- To evaluate MCT-1 as a potential therapeutic target for cancer treatment.
Main Methods:
- Investigated MCT-1's role in Shc-Ras-MEK-ERK signaling pathways.
- Analyzed MCT-1 co-activation with the Shc gene in human carcinomas.
- Performed MCT-1 knockdown experiments to assess effects on apoptosis, caspases, and caspase substrates under stress.
- Evaluated the impact of targeting MCT-1 on cancer cell proliferation, chemo-resistance, and tumorigenic capacity.
Main Results:
- MCT-1 was identified as a novel regulator of the Shc-Ras-MEK-ERK signaling pathway.
- MCT-1 is significantly co-activated with the Shc gene in human carcinomas.
- MCT-1 knockdown induced apoptotic cell death via caspase activation and substrate cleavage under stress.
- Targeting MCT-1 effectively suppressed cancer cell proliferation, chemo-resistance, and tumorigenic capacity.
Conclusions:
- An important linkage between MCT-1 oncogenicity and the Shc pathway in tumor development has been established.
- MCT-1 expression, potentially promoted by gene hyperactivation, may serve as a tumor marker.
- MCT-1 represents a promising molecular target for cancer therapy.
