RICH1 enhances pro-inflammatory TAM infiltration in breast cancer via promoting TRIM21-mediated ubiquitination of RhoA and inhibiting STAT3 phosphorylation.

ABSTRACT: Immunotherapy has emerged as an effective treatment for breast cancer, making the exploration of novel immune-related biomarkers of paramount importance. A vital aspect of this exploration is the investigation into the subtyping of tumor-associated macrophages (TAMs). While polarity proteins within TAMs can shift their functional status, the impact of polarity proteins on inflammation-related signaling in tumor cells and their subsequent influence on the tumor microenvironment (TME) remains elucidated. We discovered that RICH1, functioning as a tumor suppressor molecule in breast cancer, significantly increased the infiltration of pro-inflammatory M1-like TAMs within TME in 4T1 tumor-bearing mice. Furthermore, the conditioned medium from RICH1-overexpressing 4T1 cells promoted M1-like pola

SUBMITTER: Zhou Y 

PROVIDER: S-EPMC12855860 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature