How NOX4 Affects Cancer Formation: New Support of My Explanation of the "Warburg Effect," the Increase of Metabolism in Cancer

I suggest the basis of Hanley, et al., "Targeting the Myofibroblastic Cancer-Associated Fibroblast Phenotype Through Inhibition of NOX4," Journal of the National Cancer Institute, volume 110, Issue 1, may be reduction in availability of dehydroepiandrosterone (DHEA) for cancer cell growth.

The "Warburg Effect," which is increased metabolism of cancer may be directly affected by DHEA availability. I explain this connection in detail in: "Use Of DHEA By Cancer Explains The "Warburg Effect" ...Increased Cancer Metabolism (New Support of My Cancer Explanation)," at: http://anthropogeny.com/warburg%20effect%20cancer.html .

NOX4 has been connected to the Warburg Effect.

It is my hypothesis that DHEA exerts its actions through androgen receptors. For example this is the basis of human evolution. That is, I think increased testosterone in humans compared to the Great Apes is why our DHEA is lower than theirs but our testosterone is higher. Testosterone increases androgen receptors which increases DHEA use by human tissues, especially the brain. ("Androgens in Human Evolution," Rivista di Biologia / Biology Forum 2001; 94: 345-362.)

It has been determined that NOX4 is involved in androgen receptor expression.

Therefore, I suggest that Hanley, et al., achieved their findings by reducing NOX4, which reduces androgen receptors which would reduce tumor size as well as reducing the Warburg Effect. This could also explain why increased testosterone is connected with increased cancer, therefore, why cancer is much more common in humans compared to the Great Apes.