Abstract
Cancer treatment through immune checkpoint receptor blockade has made significant advances in the recent years. However, resistance to the current immune checkpoint inhibitors (ICIs) has been observed in many patients, who consequently do not respond to these treatments. T-cell immunoglobulin mucin-3 (Tim-3) is a novel immune checkpoint molecule emerging as a potential therapeutic target for cancer immunotherapy. Epidemiologic findings reveal that genetic polymorphisms in the Tim-3 gene are associated with increased susceptibility to breast cancer. In patients with breast cancer, Tim-3 is expressed both on immune and tumor cells. Accumulating evidence demonstrates that Tim-3 can notably affect breast cancer treatment outcome and prognosis. Therefore, Tim-3 is being regarded as a high-potential target for improving breast cancer therapy. In this review, we summarize the role of Tim-3 in breast cancer and the regulation mechanisms of Tim-3 to furnish evidences for future research and therapy.
Highlights
Breast cancer is the most common malignant tumor and the leading cause of cancer-associated mortality among women [1]
The results show that T-cell immunoglobulin mucin-3 (Tim-3) blockade enhances anti-tumor immunity by upregulating genes through means such as acetylation, cell differentiation, apoptosis, TGF-b signaling, immune response, negative regulation of angiogenesis, activation of the IFN-g-mediated pathway, and mitogenactivated protein kinase signaling that favor immune cell proliferation and activation and enhance T-cell cytotoxicity [80]
Tim-3 is broadly expressed by different types of cells in breast cancer
Summary
Breast cancer is the most common malignant tumor and the leading cause of cancer-associated mortality among women [1]. THE ROLE OF TIM-3 EXPRESSION ON IMMUNE CELLS IN BREAST CANCER Another study assessed the association of Tim-3 expression on T cells from tumor-draining lymph nodes with breast cancer progression.
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