Table 1.
Protein | Cancer outcome | DNA damage processing modulation | Ref. |
---|---|---|---|
HMGB1 | • Gastric cancer • Hepatocellular cancer • HNSCC • Nasopharyngeal cancer • Colorectal cancer • ESCC • Mesothelioma • Bladder cancer • Prostate cancer • Cervical cancer • Ovarian cancer • NSCLC |
• Promotes error-free repair via NER • Binds with high affinity to chemotherapeutic DNA lesions • Positive cooperative binding with NER damage recognition proteins on DNA lesions • Assists in recruitment of XPA to damaged DNA • Introduces negative supercoiling preferentially to damaged DNA • HMGB1 depletion increases sensitivity to DNA crosslinking agents • HMGB1 depletion results in increased DSBs |
27–31 54–64 84–105 |
HMGB2 | • HNSCC • Breast cancer • Colorectal cancer • Ovarian cancer • Gastric cancer |
• Increases γ-H2AX foci formation after damage, and delays repair | 33–38 |
HMGB3 | • Ovarian cancer • NSCLC • Colorectal cancer • Gastric cancer • ESCC • Urinary bladder cancer |
• HMGB3 depletion downregulates the ATR/CHK1 signaling pathway | 39 – 46 |
HNSCC = Head and neck squamous cell carcinoma, NSCLC = Non-small cell lung cancer, ESCC = Esophageal squamous cell carcinoma