The Immortal Cell
John Melford in Pocket Guide to Cancer, 2017
During the G2 phase, preparations are put in place for the mitosis phase that follows it. An important check is the proofreading of DNA to make sure it is accurately replicated and it is not damaged. The cell also synthesizes proteins and other cellular components needed for cell division. Perhaps the most important checkpoint function is the assessment of DNA damage carried out in the G2 phase. If any is found, the cell cycle is put on hold until repairs are carried out. If this is not possible, the cell is destroyed. Apoptosis is the mechanism by which such cells are killed, following checkpoint failure in the G1 or G2 phases. It is checkpoint failure due to irreparable DNA damage that selectively kills dividing cells during chemotherapy and radiation treatment. Quiescent cells and differentiated cells do not die in this manner.
Irradiation-induced damage and the DNA damage response
Michael C. Joiner, Albert J. van der Kogel in Basic Clinical Radiobiology, 2018
There are two checkpoints in G2, both of which operate along similar lines to that in the S phase (35). The G2 checkpoint termed ‘early’ is ATM-CHK2-CDC25A/C dependent and applies to cells that are irradiated while in G2. This checkpoint is activated by relatively low doses of radiation (1 Gy is enough) and results in a block of cell-cycle progression at the end of G2. The target of ATM-CHK2-CDC25A/C signalling in this case is the mitotic cyclinB/CDK1 complex which, like CDK2 in the S-phase, must be dephosphorylated on specific sites to become active. It is called the early G2 checkpoint because it applies to cells that are irradiated while in the G2 phase and rapidly blocks their movement into mitosis. As a result, there is a drop in the number of cells within mitosis at short times after irradiation.
Cancer Biology and Genetics for Non-Biologists
Trevor F. Cox in Medical Statistics for Cancer Studies, 2022
When a cell divides into two daughter cells, it passes through two gap phases (G1 and G2), a synthesis phase (S) and a mitosis phase (M). A brief description of the phases is: G1 phase: the cell enlarges, organelles are copied, preparation for cell divisionS phase: DNA replicatesG2 phase: the cell further enlarges, proteins and organelles are madeM phase: the splitting of the cell, first mitosis consisting of the phases: prophase, metaphase, anaphase and telophase, followed by cytokinesis where the cytoplasm of the cell is split in two, resulting in the two new cells
Açaí (Euterpe oleracea Mart.) presents anti-neuroinflammatory capacity in LPS-activated microglia cells
Published in Nutritional Neuroscience, 2022
Diulie Valente de Souza, Lauren Pappis, Thuany Teixeira Bandeira, Gabriela Geraldo Sangoi, Tuyla Fontana, Vitor Braga Rissi, Michele Rorato Sagrillo, Marta Maria Duarte, Thiago Duarte, David Frederick Bodenstein, Ana Cristina Andreazza, Ivana Beatrice Mânica da Cruz, Euler Esteves Ribeiro, Alfredo Antoniazzi, Aline Ferreira Ourique, Alencar Kolinski Machado
Cell cycle analysis was performed to understand how freeze-dried hydroalcoholic açaí extract affects microglia cell proliferation. The cell cycle is comprised of several phases, specifically S, G2, and sub-G0/G1. The S phase is responsible for DNA duplication, while G2 phase is the moment for mitosis protein synthesis followed by the cell division events. It is already known that PAMP agents, such as LPS, are capable to induce increased S and G2/M phases in cells responsible for inflammatory response, indicating cellular activation. In BV-2 cells activated with LPS, we observed an increase in the number of cells in the S and G2/M phases compared to untreated cells. However, treatment with 1 μg/mL of açaí was capable of reversing cell cycle alterations induced by LPS exposure. None of the treatments induced sub-G0/G1 status (condition related to cellular death), corroborating the results of the dsDNA release analysis. A study performed by Martinez et al. [46] found açaí increased the number of cells in the G0/G1 phases. On the other hand, Machado et al. [25] found açaí arrested cells in the S phase and confirming our results. In addition, it has been shown MG53, a member of the tripartite motif (TRIM) family protein, attenuates neuroinflammation in activated microglia cells via cell cycle arrest [47]. These results indicate that açaí extract is able to block the cell cycle at the S phase and prevent progression into the G2/M phases. Therefore, a possible mechanism of action of açaí and other anti-inflammatory agents is to inhibit the progression of the cell cycle, specifically at the S phase.
Synthesis and anticancer properties of celastrol derivatives involved in the inhibition of VEGF
Published in Journal of Enzyme Inhibition and Medicinal Chemistry, 2023
Mingxia Song, Jiantao Wen, Yi Hua, Yangnv Zhu, Qishan Xia, Qiaoyue Guo, Yiqin Luo, Xianqing Deng, Yushan Huang
Cell cycle dysregulation and uncontrolled mitosis are important causes of the infinite proliferation of cancer cells.33 Therefore, blocking the cell cycle and inhibiting the mitotic division of cells are considered to be important reasons for inhibiting cell proliferation. To explore the antiproliferative mechanism of compound 2, the effects of compound 2 on the cell cycle progression were explored by flow cytometry in the MGC-803 cell. The experimental results were shown in Figure 1. After treating cells with compound 2 for 18 h, the number of cells in the G2 phase was increased in a concentration-dependent manner (from 15.05% to 37.01%), The number of cells in the G1 phase was decreased (from 64.36% to 44.77%). The proportion of cells in the S phase was almost unchanged. While celastrol reduced the proportion of G1 phase cells (from 63.37% to 52.96%) and increased the proportion of S phase cells (from 19.18% to 29.41%). The proportion of G2 phase cells remained almost unchanged. The above results showed that compound 2 can block the cell cycle in the G2 phase, while celastrol blocks the cell cycle in the S phase.
BP-1-102 and silencing of Fascin-1 by RNA interference inhibits the proliferation of mouse pituitary adenoma AtT20 cells via the signal transducer and activator of transcription 3/fascin-1 pathway
Published in International Journal of Neuroscience, 2021
GuoDong Qian, Jian Xu, XiaoXu Shen, Yang Wang, Dong Zhao, XiaoChun Qin, Hong You, Qi Liu
Cell cycle results by flow cytometry showed that the G1 phase cell percentages in the PA, PA + DMSO and PA + BP-1-102 groups were 59.23 ± 2.01%, 59.95 ± 2.78% and 76.65 ± 1.77%, respectively. The proportion of cells in the G1 phase increased after BP-1-102 interference (Figure 6(A,C)), and the difference was statistically significant compared with the PA group (Figure 6(F)) (p < .001). The proportions of cells in the G2 phase were 25.67 ± 1.28%, 25.96 ± 0.65% and 17.65 ± 2.1%. The proportions of cells in the S phase were 15.11 ± 2.95%, 14.09 ± 2.33% and 5.69 ± 0.35% in the PA, PA + DMSO and PA + BP-1-102 groups, respectively. The proportions of cells in the G2 and S phases decreased after BP-1-102 interference (Figure 6(A,C)), and the difference was statistically significant (p < .01) compared with the PA group (Figure 6(F)). This result indicates that BP-1-102 significantly inhibits the proliferation of mouse pituitary tumor cells.
Related Knowledge Centers
- DNA
- DNA Replication
- Interphase
- S Phase
- Chromatin
- Cell Cycle
- Mitosis
- Prophase
- Chromosome
- Protein Biosynthesis