Abstract
BackgroundTo analyze the ways and methods of signaling pathways in regulating cell cycle progression of NIH3T3 at transcriptional level, we modeled cell cycle of NIH3T3 and found that G1 phase of NIH3T3 cell cycle was at 5–15 h after synchronization, S phase at 15–21 h, G2 phase at 21–22 h, M phase at 22–25 h.ResultsMouse Genome 430 2.0 microarray was used to detect the gene expression profiles of the model, and results showed remarkable changes in the expressions of 64 cell cycle genes and 960 genes associated with other physiological activity during the cell cycle of NIH3T3. For the next step, IPA software was used to analyze the physiological activities, cell cycle genes-associated signal transduction activities and their regulatory roles of these genes in cell cycle progression, and our results indicated that the reported genes were involved in 17 signaling pathways in the regulation of cell cycle progression. Newfound genes such as PKC, RAS, PP2A, NGR and PI3K etc. belong to the functional category of molecular mechanism of cancer, cyclins and cell cycle regulation HER-2 signaling in breast cancer signaling pathways. These newfound genes could promote DNA damage repairment and DNA replication progress, regulate the metabolism of protein, and maintain the cell cycle progression of NIH3T3 modulating the reported genes CCND1 and C-FOS.ConclusionAll of the aforementioned signaling pathways interacted with the cell cycle network, indicating that NIH3T3 cell cycle was regulated by a number of signaling pathways.Electronic supplementary materialThe online version of this article (doi:10.1186/s12860-015-0071-7) contains supplementary material, which is available to authorized users.
Highlights
To analyze the ways and methods of signaling pathways in regulating cell cycle progression of NIH3T3 at transcriptional level, we modeled cell cycle of NIH3T3 and found that G1 phase of NIH3T3 cell cycle was at 5–15 h after synchronization, S phase at 15–21 h, G2 phase at 21–22 h, M phase at 22–25 h
The results showed that when the cells were synchronized by the method mentioned above, the G1 phase of the cells could last for 5 h
We found that G0/G1 phase checkpoint of NIH3T3 cells was at 5 h after synchronization, G1 phase at 5–15 h, G1/S phase checkpoint at 15 h, S phase at 15–21 h, S phase checkpoint at h, G2 phase at 21–22 h, G2/M phase checkpoint at h, M phase at 22–25 h, end of M phase at 25 h
Summary
To analyze the ways and methods of signaling pathways in regulating cell cycle progression of NIH3T3 at transcriptional level, we modeled cell cycle of NIH3T3 and found that G1 phase of NIH3T3 cell cycle was at 5–15 h after synchronization, S phase at 15–21 h, G2 phase at 21–22 h, M phase at 22–25 h. NIH3T3 is a mouse embryonic fibroblasts (MEFs) cell line with a high degree of contact inhibition in continued culture. It was separated from NIH Swiss mouse embryo cultures [1], and belongs to mesenchymal stem cells (MSCs)-like multipotent progenitor cells. These cellspossess multipotency and self renewal abilities [2], and are frequently used in transfection and gene expression researches [3]. The work of Jeong et al demonstrated that 2M4VP blocked the phosphorylation of Rb by regulating the proteins
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