
-   Following DNA damage in normal p53+/+ cells, cyclin G is triggered to cluster in discrete nuclear DNA replication foci that contain replication-associated proteins such as proliferating cell nuclear antigen. While p53-/- cells displayed a faint cyclin G nuclear staining pattern, there was no increased expression and no change in distribution of the staining pattern after DNA damage [PMID: 10196184].
-   Cyclin G1 and cyclin G2 are induced by the DNA damaging agent actinomycin-D, and although the induction of cyclin G1 was p53 dependent, activation of cyclin G2 expression was observed in the absence of p53 [PMID: 8806701].
-   Results indicated that cyclin G-mediated p53 regulation is dependent upon the status of ataxia-telangiectasia mutated (ATM) protein, which activates p53 in response to DNA damage. It was also demonstrated that translocation of cyclin G to the nucleus requires functional ATM [PMID: 15077171].
-   Lung carcinoma cell lines treated with oleanolic acid (OA), a natural compound from plants with known anti-tumor activities, CCNG1 and MEF2D were found to be downregulated by OA treatment. Overall, it appeared that OA induced cell cycle arrest in lung cancer cells through miR-122/Cyclin G1/MEF2D pathway [PMID: 25472877].
-   In vitro and in vivo experiments suggested that the activation of P53mt-Notch3-CCNG1 pathway was responsible for tumor progression to advanced disease with correlation with worse prognosis in patients with HGSOC high-grade serous ovarian cancer [PMID: 30565428].
-   In human lung cells, cyclin G1 enhanced radiation sensitivity resulting in increased cell death by overriding radiation-induced G2 arrest through transcriptional upregulation of cyclin B1 in a p53-independent manner [PMID: 16322753].
-   In pancreatic ductal adenocarcinoma (PDAC) tissues, LINC01133 expression is higher in PDAC tissues compared to adjacent non-cancerous tissues, and this overexpression is associated with poorer prognosis among the patients. Higher expression of C/EBPbeta was also observed in PDAC tissues, and this overexpression was also associated with the poorer prognosis. In vitro experiments showed that that the CCAAT/enhancer-binding protein beta-LINC01133 axis performs an oncogenic function in PDAC by activating CCNG1 [PMID: 29458145].
-   Using a yeast two-hybrid screen and isolated two mouse cDNAs encoding cyclin G-interacting proteins, results indicated that cyclin G forms a specific complex with the B subunit of protein phosphatase 2A and that complex formation is regulated by p53 [PMID: 8887688].
-   Progesterone-induced cyclin G1 mediates the inhibitory effect of progesterone on endometrial epithelial cell proliferation possibly through the recruitment of PP2A to dephosphorylate Rb [PMID: 25007270].

## Summary

The CCNG1 gene, coding for Cyclin G1, is implicated in growth regulation and is associated with G2/M phase arrest in response to DNA damage [CS: 8]. Cyclin G1's role in mediating cell cycle arrest at the G2/M phase in response to DNA damage indicates its function as a safeguard against the propagation of damaged DNA [CS: 8]. In bone marrow, where hematopoietic stem cells divide rapidly, preserving genomic integrity is crucial [CS: 10]. Therefore, the upregulation of CCNG1 following toxic exposure acts as a protective mechanism, halting cell cycle progression to allow for DNA repair or to trigger apoptosis in severely damaged cells [CS: 9]. For instance, exposure to benzene and radiation, as evidenced by studies in mice, leads to an upregulation of Cyclin G1 [CS: 7]. This response is crucial in preventing the proliferation of potentially malignant cells, a risk heightened in rapidly dividing tissues like bone marrow [CS: 9].
