Cancer cell surface molecule recognized by NKG2D, NKp30, and DNAM-1 receptors

This entry refers to a collection of cancer cell surface molecules that are recognized by the activating receptors NKG2D, NKp30, and DNAM-1 on cytotoxic immune cells such as cytokine-induced killer (CIK) cells and natural killer T-like lymphocytes. These molecules are not a single target but include several families: NKG2D recognizes stress-induced proteins such as MHC class I chain-related proteins A and B (MICA/MICB) and the ULBP family. These are upregulated in many cancers but can be downregulated or shed to evade immune detection[2]. NKp30 binds to tumor-associated ligands including B7-H6, which is expressed on various primary tumors but not healthy tissues. Another ligand is BAG6/BAT3, found at the plasma membrane or in exosomes from tumor cells[2]. DNAM‑1 interacts with adhesion molecules like CD112/Nectin‑2 and CD155/PVR, which can also be upregulated in malignancy. These interactions play critical roles in anti-tumor immunity by enabling CIK/NKT-like lymphocytes to recognize and kill cancer cells. However, tumors often develop mechanisms to reduce ligand expression or release soluble forms that inhibit receptor function—posing challenges for therapeutic targeting[2]. The prognostic value of some of these ligands has been demonstrated in cancers such as colorectal and breast cancer. Because this entry groups multiple distinct molecular entities under one label without specifying an individual molecule or gene product—and because each receptor-ligand pair has unique biology—it should be considered non-canonical for structured data purposes.

Other names

NKG2D ligands (e.g., MICA, MICB, ULBP1–4)NKp30 ligands (e.g., B7-H6, BAG6/BAT3)DNAM-1 ligands (e.g., CD112/Nectin-2, CD155/PVR)

Varies depending on the specific ligand/receptor interaction; generally involves activation of cytotoxic lymphocytes against tumor cells.