Inhibition of Mitochondrial DNA Transcription as an Approach to Universal Cancer Therapy

The key to a universal cancer therapy is to find a vulnerability that is (a) common to all cancers, something fundamental to cancer as a class, (b) nowhere near as prevalent in normal cells, and (c) can be cost-effectively exploited as a basis for treatment. Lengthening of telomeres is a good example, and an area in which at least a few groups are working at an early stage. Cancer cells must employ telomerase or alternative lengthening of telomeres mechanisms to evade the Hayflick limit on replication, triggered by short telomeres, as telomere length is reduced with each cell division. Other examples include other mechanisms related to cell replication, unsurprisingly given that unfettered replication is a defining characteristic of cancer. Today's research materials discuss an interesting example of this type of approach. Researchers here note that production of proteins from mitochondrial DNA is critical to cell replication. Yet their experiments in interfering in that process demonstrate that mitochondrial gene expression is not so critical that it can't be turned off for a while in normal tissues, given a normal rate of cell division. Cancerous cells, on the other hand, with their rampant pace of replication, run into issues if their ability to produce proteins from mitochondrial DNA is impaired. Reducing the ability of cancerous cells to replicate is a promising way to improve the effectiveness of any treatment based on killing cancerous cells, and particularly if...
Source: Fight Aging! - Category: Research Authors: Tags: Medicine, Biotech, Research Source Type: blogs