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Killing Melanoma Cells More Effectively By Combining Drugs

BH3 is a protein that is needed to survive against cancer. It is present on the p53 gene. Cancer cells destroy the action of this gene. Bcl-2 gene keeps cancer cells alive. FDA has approved drugs called “BH3 mimetics” which help BH3 protein in its working example drug venetoclax is a BH3 mimetic. BH3 mimetics [...]

BH3 is a protein that is needed to survive against cancer. It is present on the p53 gene. Cancer cells destroy the action of this gene. Bcl-2 gene keeps cancer cells alive. FDA has approved drugs called “BH3 mimetics” which help BH3 protein in its working example drug venetoclax is a BH3 mimetic.

BH3 mimetics have also been used to treat skin cancer but here the drug works in a sneaky way. It has been elaborated in a journal Cell Death and Disease that how skin melanoma escapes BH3 mimetics. Protein MCL-1 is a member of the BCL-2 family. Even in the case,  Bcl-2 is turned off MCL-1 sends survival signals to melanoma.

Navitoclax is from the family of venetoclax which was used by a group to inhibit BcI-2 along with the investigational drug A-1210477. This combination killed melanoma cells along the melanoma stem cells which stopped its initiation again.

According to Nabanita Mukherjee cancer cells are a combination of pro-death and anti-death proteins. These cells live or die with respect to balance maintained between these. Combination of Navitoclax and A-1210477 eliminates anti-death proteins, consequently, cancerous cells die.

Then comes the role of another genetic player from the same family of BCL-2. DRP-1 makes death proteins in the case of breast cancer but in the case of skin melanoma, it works in the opposite way. The research group then used CRISPR/Cas9 to mute DRP-1 which killed melanoma cells. This was even better.

It is been believed that BH3 mimetics would be favored by DRP-1 inhibition to treat melanoma. Members of family BCL-2 are frequently being checked to have the most effective treatment for skin cancer patients.

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