Lysophosphatidic acid receptors (LPARs) are six G-protein-coupled receptors that mediate LPA signaling to promote tumorigenesis and therapy resistance in many cancer subtypes, including breast cancer. Individual-receptor-targeted monotherapies are under investigation, but receptor agonism or antagonism effects within the tumor microenvironment following treatment are minimally understood. In this study, we used three large, independent breast cancer patient cohorts (TCGA, METABRIC, and GSE96058) and single-cell RNA-sequencing data to show that increased tumorLPAR1,LPAR4, andLPAR6expression correlated with a less aggressive phenotype, while highLPAR2expression was particularly associated with increased tumor grade and mutational burden and decreased survival. Through gene set enrichment analysis, it was determined that cell cycling pathways were enriched in tumors with lowLPAR1,LPAR4, andLPAR6expression and highLPAR2expression. LPAR levels were lower in tumors over normal breast tissue forLPAR1,LPAR3,LPAR4, andLPAR6, while the opposite was observed forLPAR2andLPAR5.LPAR1andLPAR4were highest in cancer-associated fibroblasts, whileLPAR6was highest in endothelial cells, andLPAR2was highest in cancer epithelial cells. Tumors high inLPAR5andLPAR6had the highest cytolytic activity scores, indicating decreased immune system evasion. Overall, our findings suggest that potential compensatory signaling via competing receptors must be considered in LPAR inhibitor therapy.