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Villainous protein: The wrench in the gears of cancer growth

Researchers from the University of California - San Francisco have discovered that it is a cell protein, called RBM42, that makes the cells churn out MYC, a cancer-causing protein.

Express News Service

The war against cancer may have received a shot in the arm with a new method that appears to be a surefire one offering a potent avenue to fight the dreaded disease. The new method simulates throwing a wrench in the gears of cancer growth to prevent the cell’s protein factories from making the notorious cancer-causing protein MYC, which is the villain contributing to out-of-control tumours.

MYC is a protein produced in the cells. It is a master regulator of gene transcription and is involved in the development and progression of about 70% of cancers. MYC is a transcription factor regulating the expression of thousands of genes. It is often dysregulated in human cancers, leading to uncontrolled cell growth and tumour formation by binding to promoters in DNA which are regulatory regions that control whether genes are turned on or off.

Researchers from the University of California - San Francisco (UCSF) have now discovered that it is another cell protein, called RBM42, that makes the cells churn out MYC.

The researchers, while studying RBM42 in pancreatic cancer cells, found that disrupting this protein formation in the cells stopped the tumours from growing. They first interfered with the RBM42 in cancer cells in petri dishes, and then in mice, and in both cases, when they removed RBM42, the ribosomes stopped making MYC, and the pancreatic tumors stopped growing.

This revealed that it is RBM42 which is the Achilles’ Heel in some of the worst cancers. It is one protein clandestinely playing a role in encouraging another to proliferate cancerous growth.

The latest development throws light on the future direction of developing effective drugs that can restrict the formation of the RBM42 protein in the cells to in turn stop feeding fuel to MYC that plays its role in uncontrolled growth of cancerous tumours.

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