Gene therapy to raise levels of the natural antioxidant catalase in mitochondria is one of many methods shown to modestly extend life in mice. Cancer is so very prevalent in mice that it is frequently worth asking whether or not life extension is a matter of slowing aging or a matter of suppressing cancer - though there is certainly a lot of room for argument as to whether or not these are just two ways of stating the same thing, based on the details of the mechanisms involved. See the debate over whether rapamycin slows aging or suppresses cancer, for example. Given all this, the paper linked here is interesting:
The antioxidant enzyme catalase targeted to mitochondria (mCAT) has been shown to delay aging and cancer in mice, and the progression of transgenic oncogene and syngeneic tumors was suppressed, helping support the notion that attenuation of mitochondria-generated hydrogen peroxide signaling is associated with an antitumor effect.
In order to determine if mCAT has any effect on naturally occurring lung cancer of the adenocarcinoma type in old mice, the tumor incidence and progression were examined in the lungs of old mCAT transgenic and wild-type (WT) mice with a CB6F1 background. CB6F1 mice with a WT genotype were found to have a high incidence of adenomas at 24 months of age, which progressed to adenocarcinomas at 32 months of age. CB6F1 mice with the mCAT genotype had significantly reduced incidence and severity of lung tumors at both ages.
Fibroblasts isolated from the lungs of old mCAT mice, but not WT mice, were shown to secrete soluble factors that inhibited lung tumor cell growth suggesting that stromal fibroblasts play a role in mediating the antitumor effects of mCAT. The aged CB6F1 mouse, with its high incidence of K-ras mutant lung cancer, is an excellent model to further study the anticancer potential of mitochondria-targeted therapy.