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Focus Formation: A Cell-based Assay to Determine the Oncogenic Potential of a Gene
Published on: December 31, 2014
Sustained loss of a neoplastic phenotype by brief inactivation of MYC
Meenakshi Jain1, Constadina Arvanitis, Kenneth Chu
1Division of Oncology, Departments of Medicine and Pathology, Stanford University, Stanford, CA 94305-5151, USA.
Abstract:
Pharmacological inactivation of oncogenes is being investigated as a possible therapeutic strategy for cancer. One potential drawback is that cessation of such therapy may allow reactivation of the oncogene and tumor regrowth. We used a conditional transgenic mouse model for MYC-induced tumorigenesis to demonstrate that brief inactivation of MYC results in the sustained regression of tumors and the differentiation of osteogenic sarcoma cells into mature osteocytes. Subsequent reactivation of MYC did not restore the cells' malignant properties but instead induced apoptosis. Thus, brief MYC inactivation appears to cause epigenetic changes in tumor cells that render them insensitive to MYC-induced tumorigenesis. These results raise the possibility that transient inactivation of MYC may be an effective therapy for certain cancers.
Insights
Briefly inactivating the MYC oncogene in mice led to sustained tumor regression and cell differentiation. Reactivating MYC after this transient therapy induced apoptosis, suggesting a potential new cancer treatment strategy.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Genetics
Background:
- Pharmacological inactivation of oncogenes is a potential cancer therapy.
- Cessation of oncogene inactivation therapy may lead to tumor regrowth.
- MYC oncogene plays a critical role in tumorigenesis.
Purpose of the Study:
- To investigate the effects of transient MYC inactivation on MYC-induced tumors.
- To determine if brief MYC inactivation leads to sustained tumor regression.
- To explore the potential of transient oncogene inactivation as a cancer therapy.
Main Methods:
- Utilized a conditional transgenic mouse model for MYC-induced tumorigenesis.
- Administered brief inactivation of the MYC oncogene.
- Observed tumor regression and cell differentiation.
- Reactivated MYC to assess its effect on previously treated tumor cells.
Main Results:
- Brief MYC inactivation resulted in sustained tumor regression.
- Osteogenic sarcoma cells differentiated into mature osteocytes.
- Subsequent MYC reactivation induced apoptosis in tumor cells.
- Tumor cells became insensitive to MYC-induced tumorigenesis after transient inactivation.
Conclusions:
- Transient MYC inactivation can cause epigenetic changes leading to sustained tumor regression.
- This approach may render tumor cells insensitive to MYC's oncogenic effects.
- Brief MYC inactivation shows promise as an effective therapy for certain cancers.
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