Global Genome Repair to combat skin tumorigenesis. Is this the future of skin cancer treatment? Here is what the new study has to say.
What Is Skin Tumorigenesis?
A normal human cell is made up of nucleic acids, carbohydrates, proteins, and lipids. They also consist of various other molecules depending on their function in the body. When these original molecules are replaced by carcinogenesis molecules and progenitor cells, the cell loses its identity and transforms into a cancerous cell.
The cells present on the skin are highly likely to be replaced by these cancerous cells and thus, scientists are researching different ways to combat skin tumorigenesis.
Symptoms of Skin Tumorigenesis
The symptoms of tumorigenesis such as fast proliferation, metastasis, cell manipulation, eluding apoptosis and immunosurveillance, hyperexcitable metabolism and epigenetics, etc. These malignant cell symptoms are common cancer symptoms too.
What Is the Difference Between Carcinogenesis and Tumorigenesis?
Tumorigenesis refers to the primary stage of cancer where the cells are on the verge of becoming cancerous or metastasize into tumors. On the other hand, carcinogenesis refers to cancerous cells.
How to Combat Skin Tumorigenesis?
According to the American Skin Cancer Foundation, 9500 Americans are diagnosed with skin cancer every day. This roughly estimates that around 1 in 5 Americans are affected by skin cancer. Thus, coming up with a treatment to prevent the spread of skin cancer has been the foremost objective of many researchers.
The current study published in the National Academy of Sciences of the United States of America has introduced a new way to combat skin tumorigenesis.
As established earlier, disrupting the DNA structure of a cell and the inclusion of malignant molecules results in cancer. The deletion of the METTL14 (methyltransferase-like 14) genome expedites repairs and suppresses UVB radiation-induced skin cancer.
How Does METTL14 Function?
Global Genome Repair (GGR) is a method where mRNA cells are introduced to the body to repair damaged cells throughout the body. This method doesn’t involve transcribed DNA therefore, it removes lesions regardless of any DNA-specific sequence.
The mRNA used to combat skin cancer is scientifically named N6-methyladenosine (m6A) and METTL14 is an acute component of m6A. The study found that removing METTL14 reduced DDB2 and CRC translation. While DDB2 pertains to skin cancer, CRC refers to colorectal cancer.
The researchers also addressed how adding wild METTL14 reversed GGR and aided in increased translation of DDB2 into cancerous cells. They also tested out the inactive enzymatically mutant version which showed no results.
The study was performed on both mice and human skin cells and the results were successful. Researchers followed the same for YTHDF1, a modified transcript of m6A. It ensued in reduced DDB2 proteins. This indicated the role of METTL14 and YTHDF1 in association with skin tumorigenesis.
