CXCL12 inhibited T lymphocyte infiltration and promoted breast cancer metastasis

Abstract

Background Breast cancer (BC) is a malignant tumor with the highest incidence rate in women. This work explored the function of CXCL10 and CXCL12 in tumor metastasis. Methods CXCL12 and CXCL10 protein expression levels were assessed by IHC in breast cancer tissues. String revealed that CXCL12 interacts with CXCL10 protein molecules. The GEPIA2 database revealed that CXCL12 was negatively correlated with CXCL10. CXCL12. The effects of CXCL12 on invasion and migration were detected by scratch and transwell experiments in breast cancer cells. CD4 + T and CD8 + T cells in the inflammatory microenvironment of breast cancer patients were evaluated with the NGDC database and verified by IHC. Results CXCL12 knockdown inhibited migration and invasion and enhanced the expression and secretion of CXCL10 in BC. CXCL10 is responsible for the recruitment of CD4 + and CD8 + T lymphocytes into tumors and enhances antitumor effects. The single-cell data showed that the patients in the CXCL10 + CD4+/CD8 + T-cell group and the CXCL12-CD4+/CD8 + T-cell group had better prognoses. Conclusions CXCL12 promoted BC migration and invasion. On the other hand, CXCL12 inhibited the expression and secretion of CXCL10, further inhibiting T lymphocyte infiltration and promoting breast cancer metastasis in the TME.