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Cancer Biology and Genetics for Non-Biologists
Published in Trevor F. Cox, 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
Recent Advancements of Curcumin Analogs and Curcumin Formulations in Context to Modern Pharmacotherapeutics Perspectives
Published in Debarshi Kar Mahapatra, Cristóbal Noé Aguilar, A. K. Haghi, Applied Pharmaceutical Practice and Nutraceuticals, 2021
Animeshchandra G. M. Haldar, Kanhaiya M. Dadure, Debarshi Kar Mahapatra
Synthesized compound was found to possess selective cytotoxicity in breast cancer MCF-7 cell than normal MCF-10A cell. Annexin V/prodium iodide apoptosis analysis and cell cycle analysis by quantitation of DNA by flow cytometry reported that MCF-7 has been effectively seized by synthesized compounds at mitotic G2 phase, and after 72 h of incubation, induced apoptosis has observed. Upregulation of p53, transcription of p21, and downregulation of PLK-1 subsequently facilitate CDC2 phosphorylation which comes up with the arrest of the mitotic G2 phase.
Chemopreventive Agents
Published in David E. Thurston, Ilona Pysz, Chemistry and Pharmacology of Anticancer Drugs, 2021
The eukaryotic cell cycle can be separated into two main events, DNA replication during S Phase and mitosis during M Phase, with G1 and G2 gap events in between (Figure 12.3). Such events are highly conserved, and are correlated in such a way to ensure consecutive regeneration of the cell cycle. For example, binding of the protein Cdk1 to cyclin B allows transition from G2 phase to M 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.
Combination of PAKs inhibitors IPA-3 and PF-3758309 effectively suppresses colon carcinoma cell growth by perturbing DNA damage response
Published in International Journal of Radiation Biology, 2023
Muzaffer Dukel, Kayahan Fiskin
Western blot data suggested that PAK inhibitors in pairs induce cell cycle arrest but not for a single treatment. To confirm the effect of IPA-3, PF-3758309, and IPA-3 + PF-3758309 combination on the DNA content of SW620 and Colo 205 cells, we performed a flow cytometry assay. Flow cytometry was performed to test the cell cycle stage after SW620 and Colo 205 cells were treated with each drug alone or in a combination of IPA-3 + PF-3758309 for 48 h. We observed that PAK inhibitors treated cells appeared to have obvious G2 phase cell cycle arrest. In addition, the results show that SW620 and Colo 205 cells treated with IPA-3 + PF-3758309 combination exhibit significantly decreased G1 and S phase cells (Figure 5(B)). These results indicate that IPA-3 and PF-3758309 in pair arrest the cell cycle in the G2 phase, thus inhibiting the growth of colon cancer carcinoma 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.