Table 3.
Regulation mechanisms of NKG2DL expression in various tumors
| Tumor type | Regulation level | Regulation mechanism | Reference |
|---|---|---|---|
| 3′-Methyl cholangiosarcoma | Transcription level | IFN-γ downregulates the expression of NKG2DLH60 | [46] |
| Melanoma | Transcription level | IFN-γ triggers signal transducer and activator of transcription-1 signaling, lowers MICA mRNA expression, and blocks MICA expression in tumor cells | [47] |
| Malignant glioma | Transcription level | TGF-β was upregulated and selectively inhibited the expression of MICA and ULBP2/4 | [48] |
| Colon and prostate cancer and melanoma | Translation-level | miRNAs regulate the degradation of specific mRNAs, which are then involved in NKG2DL regulation | [53, 55, 56] |
| Human glioblastoma | Post-translational level | ULBP2 is released in the soluble form through the proteolytic activities of ADAM10 and ADAM17 | [61] |
| Malignant mesothelioma | Post-translational level | TGF-β and NKG2DL (MICA/B, ULBP1–3) on the exosome surface downregulate the expression of NKG2D on immune cells | [68] |