GPRC5A Can Be the Key to Lung Cancer

News article:
University of Texas M.D. Anderson Cancer Center (2007, November 14). Tumor-suppressor Gene For Lung Cancer Identified. ScienceDaily. Retrieved January 26, 2008, from http://www.sciencedaily.com/releases/2007/11/071113163023.htm

Primary scientific article:
Tao, Q., Fujimoto, J., Men, T., Ye, X., Deng, J., Lacroix, L. & et al. (2007, November 13 ). Identification of the Retinoic Acid – Inducible Gprc5aAs a New Lung Tumor Suppressor Gene. Journal of the National Cancer Institute, 99(22), 1668-1682.

Article citing primary article:
Sporn, M. B. (2007). A New Tumor Suppressor Gene, Selective for Lung Cancer Dartmouth. Journal of the National Cancer Institute, 99(22), 1654-1655.

Summary:

The cancer that the article addresses is lung cancer. Lung cancer causes the death of 160,000 Americans annually. The GPRC5A gene found in the mouse models which suppresses lung tumors. It could be a key for researchers attack lung cancer in humans. Mice who were found with two GPRC5A genes suppressed had lungs that developed until their second year normally. During the second year of the mouse’s life more than 75 percent developed precancerous lesions and the others developed malignancies. Mice with both GPRC5A genes was not broken developed adenomas by 10 percent; whereas, working with one gene by only 11 percent. Nonetheless, the last two groups did not found developed lung cancer. GPRC5A is a G protein-coupled receptor and the GPRC5A gene was found in human lungs more than in any other tissues. It is underexpressed in head and neck squamous cell carcinoma. GPRC5A gene is the key to developing cancer.

Some of the experiments that the researchers did in the laboratory are analysis of GPRC5A, comparison between lung cancer and normal lung tissue in human, deletion GPRC5A, and injection of GPRC5A back into the cell culture. GPRC5A got analysis with the method of RETROscript frist-strand synthesis kit by mRNA reversing the transcription-PCR to cDNA from the 100mg wet weight lung tissue one sample per mouse extracted by RNA . In addition, they did a comparison between human lung cancer and normal lung tissue of the GPRC5A gene expression to see if there is any differences in the mRNA. The result of human lung cancer level of GPRC5A mRNA was 409.4, adenocarcinoma was 189.2, squamous cell carcinoma was 30.6, small-cell lung cancer was 21.7, and carcinoid was 7.4. Unfortunately, the normal tissue decreased the well-differentiated rather than poorly differentiated adenocarcinomas. When LacZ replaced by deleting GPRC5A in the mice the result shows blue-green color detected by X-gal. The main point of knockout GPRC5A is to detect cancer by SP-A, SP-B, and proSP-C. The outcome of all samples are negative indicated by Clara cell marker CCSP, 6/7 adenomas and 3/6 adenocarcinomas detected by SP-A, 8/8 adenomas and 5/6 adenocarcinomas detected by SP-B and proSP-C. The researchers found that mice with GPRC5A absence lacked mutation in the K-RAS gene as an oncogene. Fortunately, more than half of the humans with non-small cell lung cancers do not have K-RAS due to mutations. In another experiment, they transfected GPRC5A back into the lung cancer cell lines in cell culture of H1792, HEK293F, and MDA1478 by 91%, 91%, and 68% in three cell lines. Therefore, the GPRC5A can be in humans and mice to suppress lung cancer.

Mostly both articles are pretty much the same. However the ScienceDaily article only mentions the significant point that inserted of the GPRC5A gene back into lung cancer cell lines suppresses colony formation of human lung cancer cells by 91 percent; whereas, the original article gives all three. The three cell lines are H1792, HEK293F, and MDA1478 by 91%, 91%, and 68%. Researchers now know that there are many more proteins in our body that function differently in each organ. People like us should now what is around us, what researchers are doing and discovering we might have a better cancer of surviving cancer by developing a drugs that that with cure cancers. Ligand of GPRC5A is still unknown to the researchers. The researchers wondered whether or not GPRC5A receptor is in the Noncanonical Wnt system that inhibits cell proliferation. When Wnt no longer exists in the system due to "always on" inhibiting that cannot cell survival. Since they are unclear about certain matters would they research more about GPRC5A for further study? If they had the chance to find out what the growth factor for GPRC5A is, would they be able to target medicines or treatments for those who have lung cancer?