Role of Medicinal Plants in Targeting Important Signaling Pathways in Cervical Cancer
Anne George, Oluwatobi Samuel Oluwafemi, Blessy Joseph, Sabu Thomas, Sebastian Mathew, V. Raji in Holistic Healthcare, 2017
Cell cycle and apoptosis are critical checkpoints in cancer cells. Cell cycle involves a series of events that take place in a cell leading to its division and duplication. Cell cycle check points are used by the cell to monitor and regulate the cell cycle. Apoptosis or programmed cell death is a tightly regulated process that plays important role in development, homeostasis, as well as in antiviral defense mechanism.42 Any defects in this process may lead to the development of malignant tumors.43 It is now well documented that induction of cell cycle arrest and apoptosis by anticancer agents is an important strategy for killing cancer cells. A number of medicinal plants such as Ficus religiosa,40 Quercetin,44 [6]-Gingerol,45Camellia sinensis,46,47Cinnamomum cassia,48Pycnarrhena cauliflora,49Cephalotaxus griffithii,50Vitis vinifera9,51Magnolia grandiflora (Honokiol),52 Genistein,53Zingiber officinale (6-Shogaol),54Rheum palmatum (Emodin),55Panax ginseng (Ginsenoside Rg-5),56Foeniculum vulgare,57Mimusops elengi,58 and Polygonum aviculare59 have been reported to be effective in regulating cell cycle and apoptosis.
Regulation of Cell Functions
Enrique Pimentel in Handbook of Growth Factors, 2017
The cell cycle comprises four major phases: G1, S (DNA synthesis period), G2, and M (mitosis period).31,32 The phases of the cell cycle are schematically represented in Figure 1.2. The S phase corresponds to the period of DNA replication, a process that depends on the activity of several types of DNA polymerases,33 as well as on the activity of other enzymes and factors. G1 is the gap period between M and the initiation of DNA synthesis, and G2 is the period between S and M. Cells in G2 contain double the amount of DNA than cells in G1. For most cells growing exponentially in culture, the interval between cell divisions is between 10 and 30 h. Differences in the duration of the cycle between different types of cells or different environmental conditions are mainly due to variation in the length of G1, with the duration of S (6 to 8 h) + G2 (2 to 6 h) + M (1 h) being relatively constant. In addition, there is much variability in the length of G1 among individual cells in a single population. Animal cells, both in vivo and in vitro, can also exist in a nongrowing, quiescent state during which they do not divide for long periods. Most frequently, normal cells that have ceased to grow have the G1 content of DNA. Quiescent cells may be metabolically different from cycling G1 cells and are considered to be in a distinct state, termed G0.
The Fight Against Cancer
Nathan Keighley in Miraculous Medicines and the Chemistry of Drug Design, 2020
Abnormalities in cell cycle regulation may occur at any of the four major phases, known as G1, S, G2, and M. progression through these phases of the cell cycle depends on the balance of the chemical signals that promote growth or inhibition. The G1 (gap 1) phase is where the cell grows in size and prepares for DNA replication in response to growth factors. The second phase (synthesis) is when DNA replication takes place. The next interval, once the chromosomes have been copied, is G2 phase (gap 2) where the cell prepares for division. During this interval, the cell has time to check for errors in the DNA replication, and repair any damaged copies. The final phase, M (mitosis) is when cell division happens to produce two daughter cells, each containing a full set of chromosomes. The daughter cell then begins the cell cycle at the G1 phase, or may remain in a dormant phase G0.
Synthesis and characterisation of (Z)-styrylbenzene derivatives as potential selective anticancer agents
Published in Journal of Enzyme Inhibition and Medicinal Chemistry, 2018
Ya-Bing Xin, Jia-Jun Li, Hong-Jian Zhang, Jun Ma, Xin Liu, Guo-Hua Gong, Yu-Shun Tian
The cell-cycle is a series of events that result in cell division, duplication, and proliferation. Numerous cytotoxic compounds exert their anti-proliferative effect by inducing cell-cycle arrest, apoptosis, or both2. These mechanisms are considered effective anticancer strategies21. To study the mechanism by which compound 6h reduced the viability of BEL-7402 cells, we used flow cytometry to analyse cell-cycle distribution. As shown in Figure 3(A), 6h increased the percentage of G2/M cell population in a concentration-dependent manner from 23.09% to 59.99% after 12 h incubation, and the trend was similar in the S cell population (4.44–19.35%). After treatment with 0.1 µM 6h, the cell distribution at G0/G1, G2/M, and S phases was very similar to the 0.1 µM taxol treatment group. This finding suggests that 6h induces cell-cycle arrest at the S and G2/M phases.
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.
Cell cycle inhibitors for the treatment of acute myeloid leukemia: a review of phase 2 & 3 clinical trials
Published in Expert Opinion on Emerging Drugs, 2020
Nadya Jammal, Caitlin R. Rausch, Tapan M. Kadia, Naveen Pemmaraju
Novel agents inhibiting various steps in the cascade of cell cycle signaling are currently being evaluated in the treatment of leukemia and will be discussed in this review, including studies conducted within the North American continent, as well as the UK, Japan, Australia and Europe [14]. The cell cycle consists of four phases: G1, responsible for cell growth and preparation for DNA replication; S phase, in which DNA and RNA synthesis occurs; G2, the checkpoint for DNA errors and cell division; and M phase, which is responsible for microtubule spindle assembly and cell division. Cell cycle inhibitors are agents that interfere with stepwise progression through any of these phases. Currently, a selection of potential clinically actionable targets include cyclin-dependent kinase (CDK) 4/6 and pan-CDK targeting the G1 phase, checkpoint kinase (CHK) 1 activity during the S phase, WEE1 activity in the G2 phase, and Aurora kinase activity in the M phase [14–16].