Unravelling the CXCL12/CXCR4 Axis in breast cancer: Insights into metastasis, microenvironment interactions, and therapeutic opportunities

Abstract

Breast cancer metastasis

As the second most common cause of cancer-related deaths in women, breast cancer plays a major part in the development of the disease. Resistance to chemotherapy is frequently accompanied by metastasis, a leading cause of death. Elevated in both original tumor and metastatic sites, the chemokine gene CXCL12 plays a crucial role in the metastasis of lung, ovarian, breast, and prostate cancers. Chemoresistance is a complicated issue that has intrinsic causes and adds to treatment difficulties.

Impact of the microenvironment

Drug resistance is significantly influenced by the cancer microenvironment. Chemotherapy shrinks the initial size of the tumor, while cytotoxic medicines and hormone treatment are part of standard therapy. Relapse, however, is dangerous and calls for more stringent action. Combining chemotherapy with CXCL12 receptor inhibition has demonstrated potential in saving breast cancer patients.

CXCL12 and CXCR4

The low-molecular-weight chemokine CXCL12 affects the migration of leukocytes, the development of embryos, and the spread of cancer. Its ligand, the CXCR4 receptor, is a member of the CXCR family and promotes leukocyte migration and the formation of new blood vessels. This axis is connected to inflammation, migration, and tumor invasion. Drug-resistant people have increased expression of CXCL12, which influences several biological processes via autocrine and paracrine pathways.