This study aims to investigate the expression of stress-induced phosphoprotein 1 (STIP1) in breast cancer tissues and its relationship with immune cell infiltration.

The GEPIA2 and Ualcan databases were used to analyze the expression difference of STIP1 in different types of breast cancer. Kaplan-Meier Plotter was used to analyze the relationship between the expression of STIP1 and the survival of breast cancer patients with different subtypes. TIMER database was used to analyze the correlation between STIP1 and immune cell infiltration in different types of breast cancer. The String database was used to analyze the STIP1 related interaction proteins. The difference expression of STIP1 between breast cancer and adjacent normal tissue is compared by Wilcoxon test. The difference of other indexes between two groups were compared by Mann-Whitney U test. The difference among groups were compared by Kruskal-Wallis H test, and pairwise comparisons between groups were conducted using the Dunn test. Kaplan-Meier curve was used to analyze the relapse-free survival (RFS) of STIP1 expression differences in different types of breast cancer, and Spearman correlation coefficient was used to evaluate the correlation between the proportion of immune cell infiltration and the expression level of STIP1.

Compared with normal tissues, STIP1 expression is upregulated in different types of breast cancer. High expression of STIP1 is associated with reduced RFS in breast cancer patients, especially in Luminal A breast cancer. STIP1 is positively correlated with the infiltration levels of various immune cells such as CD8⁺ T cells, CD4⁺ T cells, and neutrophils. STIP1 interacts with multiple proteins such as PTGES3, ASHA1, and PRNP, which are mainly involved in biological processes such as protein folding, protein stability, heat stress response, cell cycle, and apoptosis regulation.

The upregulation of STIP1 in breast cancer is associated with poor prognosis for patients, especially in Luminal A subtype breast cancer. STIP1 may play a significant role in the immune microenvironment of breast cancer, influencing tumor development and prognosis by modulating the functional status of immune cells.