ERRα regulates the growth of triple-negative breast cancer cells via S6K1-dependent mechanism

Targeting a protein linked to poor prognosis in breast cancer patients could help sensitize tumors to other drug therapies. A US team led by Marina Holz of Yeshiva University, New York, investigated the biochemical relationship between estrogen-related receptor alpha (ERRa) and the 40S ribosomal S6 kinase 1 (S6K1), both of which serve common functions in controlling cellular growth, proliferation and metabolism. Working with breast cancer cells in a lab dish and mouse models, they showed that ERRa binds the promoter of the gene encoding S6K1, leading to reduced gene expression. Blocking ERRa activity led to higher levels of S6K1, and these S6K1-expressing breast cancer cells were more susceptible to anti-S6K1 drugs and other agents in the same pathway. The researchers suggest that combined inhibition of ERRa and S6K1 could have therapeutic potential.