Ovarian cancer cells are "addicted" to a family of proteins produced by the notorious oncogene, MYC, and blocking these Myc proteins halts cell proliferation in the deadliest cancer of the female reproductive system, according to a presentation by University of California, Berkeley scientists at the American Society for Cell Biology (ASCB) 48th Annual Meeting, Dec. 13-17, 2008 in San Francisco.
In 30-60 percent of human ovarian tumors, MYC is overly active, or amplified, usually as a result of extra chromosomal copies of the cancer-causing gene. The extra MYC encourages the ovarian cells to manufacture too much c-Myc, a protein that regulates other genes involved in cellular growth and proliferation. The presence of excessive c-Myc protein drives healthy cells down the cancer development pathway.
Using RNA interference (RNAi) to block c-Myc protein, Berkeley scientists, Tulsiram Prathapam and G. Steven Martin, treated lab cultures of human ovarian cancer cells that contained amplified MYC. RNAi's blocking of the c-Myc protein stopped the cancer cell cycle in its tracks.
But RNAi blocking of c-Myc protein in lab cultures in which the MYC gene was not experimentally amplified did not affect ovarian cancer cell growth.
The scientists suspect that even when c-Myc was blocked in non-amplified cells, other forms of the protein ⎯ L-Myc and N-Myc ⎯ likely were present and continued to maintain cell proliferation.
By using small interfering RNA (siRNA) to silence L-Myc and N-Myc, the researchers succeeded in shutting down the growth of the non-amplified MYC tumors.