BTApep-TAT peptide inhibits ADP-ribosylation of BORIS to induce DNA damage in cancer.

ABSTRACT:

Background

Brother of regulator of imprinted sites (BORIS) is expressed in most cancers and often associated with short survival and poor prognosis in patients. BORIS inhibits apoptosis and promotes proliferation of cancer cells. However, its mechanism of action has not been elucidated, and there is no known inhibitor of BORIS.

Methods

A phage display library was used to find the BORIS inhibitory peptides and BTApep-TAT was identified. The RNA sequencing profile of BTApep-TAT-treated H1299 cells was compared with that of BORIS-knockdown cells. Antitumor activity of BTApep-TAT was evaluated in a non-small cell lung cancer (NSCLC) xenograft mouse model. BTApep-TAT was also used to investigate the post-translational modification (PTM) of BORIS and the role of BORIS in DNA damag

SUBMITTER: Zhang Y 

PROVIDER: S-EPMC9344678 | biostudies-literature | 2022 Aug

REPOSITORIES: biostudies-literature