Abstract
BACKGROUND: LSM4 belongs to the LSM (Like-Sm) gene family; however, its role in triple-negative breast cancer (TNBC) progression remains mostly unclear. Consequently, this study aimed to explore the mechanistic importance of LSM4 as a regulatory element in the progression of TNBC. METHODS: The expression of LSM4 was found to be evaluated through various bioinformatics approaches. To assess the prognostic significance and predictive capacity of LSM4, we employed univariate Cox, multivariate Cox, and nomogram models. Gene Ontology (GO) techniques were utilized to pinpoint signaling pathways linked with genes that co-express LSM4. Subsequently, LSM4 expression in clinical samples and cells was confirmed using western blotting, quantitative real-time polymerase chain reaction (qPCR), and immunofluorescence staining. The functional role of LSM4 was further examined through flow cytometry and transwell assays. Additionally, we explored the possible interaction between LSM4 and ECT2 using a combination of bioinformatics analysis and western blot assays. Rescue experiments demonstrated that the mechanism by which LSM4 enhances TNBC cell proliferation, migration, and invasion involves the AKT/PI3K signaling pathway. RESULTS: Our research demonstrated a notable increase in LSM4 expression in samples TNBC when contrasted with normal samples, and LSM4 has been recognized as a possible prognostic indicator for individuals diagnosed with TNBC. Mechanistically, the tumor-promoting influence of LSM4 on TNBC cell proliferation, migration, and invasion has been demonstrated to be enhanced by the PI3K/AKT pathway. Furthermore, our findings indicate that LSM4 can regulate the migration and invasion of TNBC cells through ECT2. CONCLUSIONS: Our findings indicate that LSM4 can play a crucial role in TNBC progression, underscoring its potential as a therapeutic target in TNBC.