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The non-enzymatic RAS effector RASSF7 inhibits oncogenic c-Myc function
Anbarasu Kumaraswamy1, Anitha Mamidi1, Pavitra Desai1
1From the National Cancer Tissue Biobank, Laboratory of Molecular Cell Biology and.
The Journal of Biological Chemistry
|August 25, 2018
Summary
Ras-association domain family member 7 (RASSF7) destabilizes the oncogenic c-Myc protein, inhibiting its function and cancer-promoting activities. This discovery offers new therapeutic strategies for targeting c-Myc in human cancers.
Area of Science:
- Oncology
- Molecular Biology
- Cell Biology
Background:
- c-Myc is a proto-oncogene crucial for cell growth and differentiation, but its role in cancer makes it a challenging therapeutic target.
- Understanding the regulation of c-Myc is vital for developing effective cancer treatments.
Purpose of the Study:
- To investigate the role of Ras-association domain family member 7 (RASSF7) in regulating c-Myc function.
- To explore the potential of targeting c-Myc through RASSF7-mediated mechanisms.
Main Methods:
- Utilized HEK293T and HeLa cell lines to study protein interactions and degradation pathways.
- Investigated RASSF7's effect on c-Myc polyubiquitination, degradation, and promoter occupancy.
- Analyzed gene expression correlations in human cancers and peptide inhibition assays.
Main Results:
- RASSF7 destabilizes c-Myc by promoting its polyubiquitination and degradation via Cullin4B.
- RASSF7 competes with MYC-associated factor X (MAX) for c-Myc binding, reducing c-Myc's transcriptional activity.
- RASSF7 inhibits c-Myc-driven oncogenic transformation, with an inverse correlation observed between RASSF7 and c-Myc expression in human cancers.
- RASSF7's leucine zipper (LZ) domain peptide can inhibit c-Myc function.
Conclusions:
- RASSF7 acts as a negative regulator of c-Myc, impacting cell proliferation and tumorigenesis.
- The RASSF7-c-Myc interaction presents a novel therapeutic strategy for targeting the oncogenic c-Myc protein.
- RASSF7's LZ domain peptide shows promise as a potential therapeutic agent against c-Myc-driven cancers.
Keywords:
MAXMyc (c-Myc)Peptide inhibitorRASSF7Ras effectorsRas proteincancercell cyclecell proliferationcell-penetrating peptide (CPP)colony forming assaytranscription factortumor cell biologytumor suppressor geneubiquitination (ubiquitination)More Related Videos
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