A lincRNA promotes TNBC growth by activating the kinases AKT and ERK through an mTORC2 component.

A Purdue University team led by Kyle Cottrell has discovered a new therapeutic target for triple-negative breast cancer. “Triple-negative breast cancer is a particularly deadly form of breast cancer ...

Emerging research suggests that environmental contaminants may influence the risk of breast cancer, particularly through exposure to endocrine disruptors and carcinogens present in the air, water, and consumer products. In a recent study, Borowsky and colleagues conducted a case-case study in Florid …

NK cells are important for the anti-tumour immune response for their potential to kill MHC class I-deficient tumor cells, but they often become dysfunctional in the immune-hostile tumour microenvironment. Here, using single-cell RNA sequencing, we identify an NK cell subpopulation that is specific to triple-negative breast cancers (TNBC) subtype, characterised by the expression of the long non-coding RNA UGDH-AS1. In these NK cells, UGDH-AS1 encodes the micropeptide, NKSM, which renders these NK cells dysfunctional due to the loss of their activation program, which leads to cancer progression. Conditional NKSM knock-in into NK cells of mice results in NK cell deactivation and increased growth of transplanted tumours. Targeted NKSM therapy effectively reduces tumor growth in TNBC mouse models. We find that UGDH-AS1+ NK cells are shaped by the tumor microenvironment (TME). Following upregulation by the TGF-β signaling pathway, NKSM binds to Myc, inhibiting its ERK1/2-mediated phosphoryla