Blocking PCNA interaction with NKp44 enhances primary natural killer cell-mediated lysis of triple-negative breast cancer cells.

Among the innate immune cells, natural killer cells (NK) serve its role in cytolytic targeting against infected and cancerous cells. NK function is regulated by an intricate balance of signals from interactions between activating and inhibitory NK receptors and ligands expressed on target cells. As an immune evasion strategy, cancer cells, particularly triple-negative breast cancer cells (TNBCs), express ligands that interact with NK receptors to inhibit NK cell cytolytic function.

Role of LLT1 and PCNA as Natural Killer Cell Immune Evasion Strategies of HCT 116 Cells.

Background/aim: Cancer stem cells (CSCs) are a subpopulation of cells that retain self-renewal and pluripotency capabilities, are resistant to chemotherapy, and are thought to facilitate metastasis. Target cell expression of proliferating cell nuclear antigen (PCNA) or lectin-like transcript 1 (LLT1) inhibits natural killer (NK) cell functions. The purpose of this study was to characterize the expression of LLT1 or PCNA as NK cell evasion strategies of HCT 116, a colorectal cancer cell line.

Lectin-like transcript 1 as a natural killer cell-mediated immunotherapeutic target for triple negative breast cancer and prostate cancer.

Breast and prostate cancer are the leading causes of death in females and males, respectively. Triple negative breast cancer (TNBC) does not express the estrogen receptor, progesterone receptor, or human epidermal growth factor receptor 2, resulting in limited treatment options. Androgen deprivation therapy is the standard care for prostate cancer patients; however, metastasis and recurrence are seen in androgen-independent prostate cancer.

2B4 (CD244, SLAMF4) and CS1 (CD319, SLAMF7) in systemic lupus erythematosus and cancer.

Signaling Lymphocyte Activation Molecule (SLAM) family receptors are expressed on different types of hematopoietic cells and play important role in immune regulation in health and disease. 2B4 (CD244, SLAMF4) and CS1 (CD319, CRACC, SLAMF7) were originally identified as NK cell receptors regulating NK cell cytolytic activity. 2B4 is expressed on all NK cells, a subpopulation of T cells, monocytes and basophils.

Blocking LLT1 (CLEC2D, OCIL)-NKRP1A (CD161) interaction enhances natural killer cell-mediated lysis of triple-negative breast cancer cells.

Triple-negative breast cancer (TNBC) is the most invasive form of breast cancer due to an absence of estrogen (ER), progesterone (PR), and human epidermal growth factor-2 (HER2) receptors on the cell surface. TNBC accounts for approximately 12 to 20 percent of all breast cancer cases. The absence of ER, PR, and HER2 receptors on TNBCs and its ability to develop drug resistance renders it difficult to eradicate or retrogress tumor growth with hormonal therapy and chemotherapy.

CS1 (SLAMF7, CD319) is an effective immunotherapeutic target for multiple myeloma.

CS1 (also known as CD319, CRACC and SLAMF7) was identified as an NK cell receptor regulating immune functions. It is also expressed on B cells, T cells, Dendritic cells, NK-T cells, and monocytes. CS1 is overexpressed in multiple myeloma and makes it a target for immunotherapy.