Effects of the MYC oncogene antagonist, MAD, on proliferation, cell cycling and the malignant phenot

Author:  ["Jun Chen","Timothy Willingham","Linda R. Margraf","Nicole Schreiber-agus","Ronald A. Depinho","Perry D. Nisen"]

Publication:  Nature Medicine

CITE.CC academic search helps you expand the influence of your papers.

Tags:     Medicine

Abstract

To investigate how overexpression of MAD, an antagonist of MYC oncogenes influences the malignant phenotype of human cancer cells, an adenovirus vector system was used to transfer the human MAD gene (AdMAD) into human astrocytoma cells. Decreased growth potential of AdMAD-infected cells was evidenced by a decrease in [3H]thymidine incorporation, an increase in cell doubling time and alteration of cell-cycle distribution. Diminished malignant potential of AdMAD-infected cells was manifested by their loss of anchorage-independent growth in soft agar and by their inability, in general, to induce tumorigenesis in a xenograft animal model. These studies indicate that adenovirus constructs encoding MAD dramatically inhibit the proliferation and tumorigenicity of human astrocytoma cells and support the use of MAD for gene therapy of human tumours.

Cite this article

Chen, J., Willingham, T., Margraf, L. et al. Effects of the MYC oncogene antagonist, MAD, on proliferation, cell cycling and the malignant phenotype of human brain tumour cells. Nat Med 1, 638–643 (1995). https://doi.org/10.1038/nm0795-638

View full text

>> Full Text:   Effects of the MYC oncogene antagonist, MAD, on proliferation, cell cycling and the malignant phenot

Intracellular expression of antibody fragments directed against HIV reverse transcriptase prevents H

Non-enzymatically glycated tau in Alzheimer's disease induces neuronal oxidant stress resulting in c