Table 2.
Different oncogenes present on ecDNA and their functions
| Cancer type | Associated gene(s) on ecDNA | Function | Refs. |
|---|---|---|---|
| Glioblastoma | MYC, EGFR, PDGFRα, ERBB2, CDK4, MDM2, KIT, MET | Increasing tumor invasiveness, radiation resistance, and drug resistance by upregulating a variety of oncogenes. In some cases, EGFRvIII and MDM2 amplification leads to Erlotinib resistance | [9, 43, 66, 90, 108] |
| Colon | DHFR, c-MYC, BRCA1 | Silencing BRCA1 gene decreased the number of DM-amplified oncogenes and the number of DM copies in ecDNA by down-regulating DHFR. In addition, MTX-resistant cells containing DM increased susceptibility to MTX | [9, 41, 71, 109, 110] |
| Neuroblastoma | MYCN | The chromosomal genome needs to be remodeled, amplified, TERT stimulated, DCLK1 inhibited, and the presence of MYCN eliminated on ecDNA to increase HU sensitivity | [75, 99] |
| Cervical | DHFR | Promoting MTX resistance by DHFR amplification | [111] |
| Ovarian | MYCN, EIF5AR, CA125 | Decreased levels of ecDNA-form CA125 after HU | [66, 108, 112] |
| Breast | DHFR, HER2 | Induced resistance to MTX by DM-form amplified DHFR is not affected by the loss of HER2 on ecDNA and trastuzamab therapy | [9, 73, 113] |
| Leukemia | c-MYC | Drug sensitivity ptomotion by down-regulating the c-MYC | [114] |
| Oral squamous cell carcinoma | MDR1 | Enhancing HU sensitivity by Loss of MDR1 | [9, 115] |