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Distinguishing friend from foe in the battle against cancer

ctive Hunter and Verma labs moved those mouse studies to the next level by tinkering with TSC activity in human cancer cells. Says Ghosh, "We were able to extend this model based on TSC null cells to different human cancer cell lines, where we knocked down TSC expression and showed that the same pattern held true."

Specifically, the team found that human cells lacking TSC genes were vulnerable to chemotherapeutic attack because they couldn't activate a major line of defense mediated by the Nuclear Factor kappa B, known as NF-kB, which triggers both inflammatory and survival responses by inducing transcription of specific genes.

Not only did this explain why TSC null cells are vulnerable to insult, but it also provided biochemical evidence that there is crosstalk between two survival mechanisms. Explains Tergaonkar, who is now an assistant professor at the Institute for Molecular and Cell Biology (IMCB) in Singapore, "Our findings show for the first time that the TSC complex can regulate the NF-kB signaling cascade."

The experiments also explained a paradox: TSC null cells treated with rapamycin actually survived cellular insult better than untreated cells-a highly inauspicious outcome if the goal is to kill cancer cells. The Hunter and Verma team found that rapamycin did that by increasing NF-kB activity in the TSC null cells when they were exposed to chemotherapeutic drugs.

Rapamycin, an immunosuppressant used to block organ rejection after transplants, also inactivates proteins stimulating cell division and in clinical trials has been combined with other drugs to halt cancer cell growth.

But to cancer cells, rapamycin is both friend and foe. "Rapamycin is not as successful as initially expected in treating cancer," explains Ghosh. "Instead of killing cells, you end up triggering a survival response in them." This study, however, suggests that taking NF-kB out of the game would make rapamycin less "friendly."

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Source:Salk Institute


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