Photo credit: Pixabay / CC0 Public Domain

Scientists at the VCU Massey Cancer Center have identified a protein that, along with a specific genetic mutation, stimulates the growth of lung cancer and could serve as a therapeutic target for the treatment of the disease.

Mutations in the p53 gene are found in more than half of all cancers, but it remains difficult to effectively fight the gene with drugs decades after it was discovered. Although previous research has shown that p53 acts as a tumor suppressor and induces cancer cell death in its natural state, a new study by Sumitra Deb, Ph.D., suggests that gain-of-function mutations (GOF) – a type of mutation that changed that Gene has an additional function – turn p53 into an oncogene, causing cells to replicate uncontrollably and contribute to the development of cancer.

Recently published in Nature Communications, the researchers found that mutant p53 genes are enabled by a specific protein, PLK3, to copy their genetic code and promote the proliferation of tumor cells through a process called transactivation.

Using preclinical models of lung cancer caused by p53 GOF mutations, Deb and his team of researchers discovered that PLK3 activates an amino acid called serine 20 (S20), a cellular building block they found to play an important role in the replication of cancer cells plays a role.

By inhibiting PLK3 in GOF p53 mutant cells, they observed a decrease in the function of S20 along with a general decrease in transactivation and tumor cell formation.

“Our research shows that GOF p53 uses PLK3 to trigger its transactivation ability and perform oncogenic functions, increasing the possibility of using PLK3 inhibitors to target p53-gated cancer cells,” said Deb, a member of the cancer biology research program at Massey and Professor in the Department of Biochemistry and Molecular Biology at the VCU School of Medicine.

Deb’s team will continue to investigate the potential of PLK3 inhibitors to be effective drugs in the treatment of lung cancer and possibly other forms of diseases with the same genetic mutation.

Scientists discover mutations that make cancer resistant to therapies against KRAS

More information:
Catherine A. Vaughan et al., Oncogenicity of Tumor-Derived Mutant p53 Increased by Recruitment of PLK3, Nature Communications (2021). DOI: 10.1038 / s41467-021-20928-8 Provided by Virginia Commonwealth University

Quote: Scientists identify protein that could serve as a therapeutic target in lung cancer (2021, April 19), accessed April 19, 2021 from cancer.html

This document is subject to copyright. Except for fair trade for the purpose of private study or research, no part may be reproduced without written permission. The content is provided for informational purposes only.