The Downregulation of CRIF1 Exerts Antitumor Effects Partially via TP53-Induced Glycolysis and Apoptosis Regulator Induction in BT549 Breast Cancer Cells.

ABSTRACT:

Background/objectives

Mitochondrial oxidative phosphorylation (OXPHOS) has been exploited as a therapeutic target in cancer treatments because of its crucial role in tumorigenesis. CR6-interacting factor 1 (CRIF1), a mitochondrial ribosomal subunit protein, is essential for the regulation of mitochondrial OXPHOS capacity. However, the mechanism of CRIF1 in triple-negative breast cancer (TNBC) cells remains unclear.

Methods/results

We showed that the downregulation of CRIF1 reduced cell proliferation in the TNBC cell lines MDA-MB-468, MDA-MB-231, and, especially, BT549. In addition, wound scratch and Transwell assays showed that CRIF1 deficiency inhibited the migration and invasion of BT549 cells. CRIF1 downregulation resulted in the suppression of mitochondrial bioenergetics

SUBMITTER: Piao S 

PROVIDER: S-EPMC11639960 | biostudies-literature | 2024 Dec

REPOSITORIES: biostudies-literature