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. 2022 Sep 9;13:968755. doi: 10.3389/fimmu.2022.968755

Table 1.

Substrates of TRIM21 involved in cancer treatments.

Model Substrate Function Manner Reference
Hepatoma cell lines HBx protein HBV replication suppression (72)
Cervical cancer cells IFI16 Cell pyroptosis inhibition and self-escape from immune surveillance K33-linked (73, 74)
HCT116 and U87 cells CLASPIN Replication fork instability and tumorigenesis K63-linked (108)
Pancreatic and colon cancer cells Par-4 Increased cisplatin resistance (110)
Osteosarcoma cells TXNIP Decreased p21 expression (105)
Colorectal cancer cells Oct-1 Sensitive to chemoradiation (122)
Primary mouse hepatocytes, hepatoma cells PXR Impaired drug–drug interactions (125)
293T cells p62 Nrf2 redox pathway inhibition the cell death induction K63-linked (130)
Bladder cancer cells PTMA p62 and Nrf2 expression inhibition (134)
Nasopharyngeal carcinoma SGSM1 MAPK pathway activation and metastasis Lys349 Lys352 (136)
Breast cancer cells SET7/9, SALL4 Tumorigenesis inhibition Lys190 in SALL4 (137, 138)
Breast cancer cells Snail EMT inhibition (139)
Breast cancer cells TβRII TGF-β signaling pathway inhibition (140)
Lung cancer cells C/EBPa Cells proliferation inhibition (141)
Glioma cancer cells CREB Tumorigenesis inhibition (142)

Multiple ubiquitination substrates of TRIM21 have been identified involved in cancer treatments.