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Micronutrients for Improved Management of Huntington’s Disease
Published in Kedar N. Prasad, Micronutrients in Health and Disease, 2019
Cell cycle progression is delayed in S-phase and G2/M phase, and enhanced apoptosis in a cell culture model of HD (STsdh (Q111)/Hdh (Q111) striatal cells compared with control cells (STsdh (Q7)/Hdh (Q7).48 Furthermore, decreased expression of miR-432, miR-146a, and miR-19a increased the levels of PCNA (proliferating nuclear antigen), CHEK1 (check point1), and CCNA2 (cyclin A2) in the primary cortical neurons expressing mutant N-terminal huntingtin protein (HTT), R6/2 mice, an animal model of HD, and HD cell model of striatum (STsdh (Q111)/Hdh (Q111). Increased expression of the above microRNAs in these striatal cells may prevent cell-cycle arrest and apoptosis.
Underlying mechanisms of apoptosis in HepG2 cells induced by polyphyllin I through Fas death and mitochondrial pathways
Published in Toxicology Mechanisms and Methods, 2020
Yawen Zeng, Zhiqin Zhang, Wenping Wang, Longtai You, Xiaoxv Dong, Xingbin Yin, Changhai Qu, Jian Ni
In order to study the effect of Polyphyllin I on cell cycle distribution, HepG2 cells were stained by PI staining and analyzed by flow cytometry. Polyphyllin I treatment resulted in an accumulation of cells in G2/M phase, accompanied by a reduction of cells in the S phase and G0/G1 phase. When compared with untreated cells, the percentage of cells in the G2/M phase increased significantly from 10.72 ± 1.11% to 28.34 ± 8.43%, while the percentage of cells in the G1/G0 phase and S phrase decreased from 57.49 ± 2.48% to 48.08 ± 3.11%, and from 31.79 ± 1.38% to 23.57 ± 8.21%, respectively (Figures 6(A,B)). Furthermore, the expression levels of proteins involved in G2/M progression were measured. The results showed that the expression levels of cyclin E1, p53 and p21 proteins were significantly up-regulated in a dose-dependent manner, while other proteins (cyclin A2 and CDK2) were significantly down-regulated (Figure 6(C)). The data revealed that Polyphyllin I could block HepG2 cells in G2/M phase.
Obacunone reduces inflammatory signalling and tumour occurrence in mice with chronic inflammation-induced colorectal cancer
Published in Pharmaceutical Biology, 2020
Xiaoping Luo, Zhilun Yu, Bei Yue, Junyu Ren, Jing Zhang, Sridhar Mani, Zhengtao Wang, Wei Dou
The cell cycle is precisely controlled by specific proteins, including P21, cyclin A2, and cyclin E1. P21, a tumour suppressor gene, is involved in the regulation of cell proliferation by inhibiting the cyclin-dependent kinase (CDK) complex (Karimian et al. 2016). Cyclin A plays a role in the rate-limiting step for entry into mitosis and its overexpression accelerates the G1 to S transition causing DNA replication (Furuno et al. 1999). Accumulation of cyclin E at the transitional period of G1-S accelerates cells entry into the S phase (Lundberg and Weinberg 1998; Ewen 2000). We, therefore, performed immunoblot analysis of the protein levels of P21, cyclin A2, and cyclin E1 in Caco2 cells. Our results showed a significant increase in the P21 protein level after obacunone treatment (Figure 8(C)). Conversely, we observed a markedly decrease in cyclin A2 and cyclin E1 protein levels in Caco2 cells. Similarly, obacunone exerted prominently suppressive effects on mRNA levels of cell proliferation-related genes (CCNA2, CCND2, CCND3, CCNE1, CCNE2, CDK2, and P21; Figure 8(D)).
Bioinformatic Identification of Hub Genes and Analysis of Prognostic Values in Colorectal Cancer
Published in Nutrition and Cancer, 2021
Xinyi Lei, Jing Jing, Miao Zhang, Bingsheng Guan, Zhiyong Dong, Cunchuan Wang
The cyclin A2 (CCNA2) which encodes protein belongs to the conserved cyclin family, whose function is considered as the regulator of cell cycle. It is well-known that CCNA2 is expressed in mammalian cells and is important for the onset of DNA replication (S phase) and mitosis by activating CDK2 and CDK1 (23,24). Prior research had shown that over-expression of cyclin A could be detected in cancers, such as cervical cancer, breast cancer, lung cancer, gastric cancer, liver cancer, and so on (25–29). The CCNA2 was expressed in growth somatic cells, and disruption of CCNA2 would cause early embryonic lethality (30,31). Previous study indicated that cyclin A2 could promote migration of HTR8 cells by the Rho-ROCK signaling pathway. Meanwhile, cyclin A2 could increase HTR8 cells’ proliferation and inhibited HTR8 cells’ apoptosis by P53 signaling pathway which was associated with DNA damage (32). In our study, CCNA2 was up-regulated in CRC samples. The recent research showed that the expression of CCNA2 was higher in CRC samples than normal samples. The cyclin A2 could promote G2/M phase transition, and knockdown of cyclin A2 could impair cell progression and lead to cell cycle apoptosis (33). CCNA2 was regarded as the cancer-promoting genes of CRC. Interestingly, our results revealed that colon carcinoma patients with high expression levels of CCNA2 had a better prognosis, compared to other research, which showed that high expression of CCNA2 had worse prognosis in lung carcinoids (34). Different results may be related to the source and quantity of tumor samples, meanwhile the molecular mechanism and signal pathway of CCNA2 in different types of tumor is awaited to be further discussed.