Table II.
Medical intervention via targeting cyclin G1 (CCNG1) for cancer therapy.
| Modes of medical intervention | Description of mechanisms, efficacy, conclusions | (Refs.) |
|---|---|---|
| Mx-dnG1 (Rexin-G): Dominant-negative | √ Apoptosis of transduced cancer cells | (90–101) |
| mutant construct of cyclin G1 (dnG1) | √ Potent tumor anti-angiogenic activity | |
| delivered intravenously by means of a | √ Broad spectrum antitumor activity | |
| tumor-targeted retroviral expression vector | √ Single-agent efficacy, long-term survivors | |
| CCNG1-suppressive oligonucleotides: | Suppression of cyclin G1 protein expression | |
| • CCNG1 antisense fragments: | √ Induces apoptosis in cancer cells, tumors | (54–56) |
| • Suppressive RNA, miR 122: | √ Induces apoptosis in cancer cells, tumors; | (105–109) |
| • siRNA-mediated CCNG1 knockdown: | √ Increases sensitivity to DOX via apoptosis; | |
| • Suppressive RNA, miR-27b | √ Inhibits cell invasion/metastatic phenotype | |
| • Suppressive RNA, miR-23b | √ CCNG1 depletion enhances taxane toxicity | (129) |
| √ Regulates multidrug resistance in gastric Ca. | (130) | |
| √ Induces apoptosis, suppresses tumorigenesis, cancer progression and metastasis | (131,132) | |
| Cytotoxic peptide drugs: | ||
| • ELAS1 peptide (cyclin G1 C-terminus): | √ Induces apoptosis, CPT chemosensitization | (133,140) |
| • Toxic a5 Helix peptides (cyclin box): | √ Induces apoptosis, necrosis, antitumor action | (136–138) |