Kidney Cancer Caused by "Sleeping Gene"? Rise and Shine!!!!

News Article:
Mayo Clinic (2007). Reactivating a Critical Gene Lost in Kidney Cancer Reduces Tumor Growth. Retrieved from http://www.sciencedaily.com/releases/2007/08/070815120439.htm


Primary Scientific Article:
Gumz, M.L. et al. (2007) Secreted Frizzled-Related Protein 1 Loss Contributes to Tumor Phenotype of Clear Cell Renal Cell Carcinoma. Clinical Cancer Research; 13(16)

This article has been cited by:

Morris, M.R. et al. (2008) Fundamental Epigenomics Approach to Identify Methylated Candidate Tumor Suppressor Genes in Renal Cell Carcinoma. British Journal of Cancer 98, 496-501

Rubin, J.S., Bottaro, D.P. (2007) Loss of Secreted Frizzled-Related Protein-1 Expression in renal Cell Carcinoma Reveals a Critical Tumor Suppressor Function. Clinical Cancer Research 13; 4660-4663



Could this be? Is the idea of having a “sleeping” gene a true one? Well in short the answer is yes. Secreted Frizzled-Related Protein 1, more commonly known as sFRP1, is a critical protein that has been found dormant or silent in clear cell renal carcinoma. Clear cell renal carcinoma or ccRCC is the most frequently occurring form of kidney cancer and the occurrences are increasing each year. Not only is it a common kidney cancer, but it has shown a resistance to radiation and chemotherapy therefore making it extremely difficult to treat. Obviously this called for a close examination of the molecular activity taking place in this type of cancer. This is what led researchers at the Mayo Clinic in Florida to conduct a study on the topic.

Normally, sFRP1 functions as a tumor suppressor gene that stops the WNT signaling pathway, which in turn would prevent an oncogenic signal chain from continuing uncontrollably. This would also prevent tumor growth and metastisis, which would occur due to the invasive nature of cancer cells. Unfortunately, through a process called methylation, proteins and transcription factors are blocked and unable to activate genes. This is to say that sFRP was never “turned on”. Therefore, in discovering the inactivity of sFRP1 in ccRCC scientists hypothesized a causational relationship between the protein inactivity and tumor growth. Furthermore, this would mean that reactivating sFRP1 would stop tumors from growing and even eliminate existing ones.

Were researchers able to prove this? The answer is yes. Researchers transfected the sFRP1 gene into human renal cancer cells. This allowed them to reactivate sFRP1 in human, animals, and tumors did in fact stop growing. Science Daily offered a brief yet accurate synopsis of the major findings by the research done at the Mayo Clinic. Basically they pointed out a few methods used to examine levels of sFRP1 from patient samples. Researchers found with one sample that the gene expression of sFRP1 was low. In another sample they saw low levels of sFRP1 mRNA, which is needed for the production of sFRP1. Lastly they point out that there was a comparison made between normal and cancerous cells. The vast majority of these cancerous samples exhibited a loss of sFRP1.

On the other hand, what is better than getting the information directly from the people who conducted the research? The researchers offer a detailed and concise step by step portrayal of the study and the findings. It is so detailed that the study can be duplicated just from reading the article. This is in fact the most trustworthy source for information on the issue. These findings open the door for treatment development for ccRCC and maybe other cancers. They may also lead to further research to answer questions about preventative measures and in which stages of the disease will reactivating sFRP1 be effective.