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The Scientific Basis of Medicine
Published in John S. Axford, Chris A. O'Callaghan, Medicine for Finals and Beyond, 2023
Chris O'Callaghan, Rachel Allen
In order to divide successfully, a cell must copy its DNA so that each daughter cell receives its full set of chromosomes. This is achieved by a tightly regulated mitosis following the cell cycle pathway (Figure 2.6). Passage through the cell cycle is controlled by cyclin proteins, in a cascade of phosphorylation events. Each cyclin acts as a catalytic subunit in partnership with a cyclin-dependent kinase (CDK). Upon cyclin binding, CDKs phosphorylate target proteins that are required for cell-cycle progression. CDK-specific inhibitors (CDKIs) bind cyclin–CDK complexes to regulate their activity and can themselves be regulated by other proteins. During mitosis, one member of each chromosome pair becomes attached to a centriole. Centrioles move to opposite ends of the cell, taking the chromosomes with them. In order to prevent inappropriate proliferation of cells, mitosis is tightly controlled, with various checkpoints to ensure that every part of the mitotic process is completed correctly before the next stage begins. Because uncontrolled proliferation is a hallmark of cancer, the cell cycle provides an obvious target for therapy. CDKIs often act as tumour suppressors and are potentially useful anticancer agents.
Oncogenesis and Metastasis
Published in Karl H. Pang, Nadir I. Osman, James W.F. Catto, Christopher R. Chapple, Basic Urological Sciences, 2021
Checkpoints control cell cycle progression.Inappropriate passage causes errors within the cell and its genetic content.
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
Frederik Roos et al.51 investigated that the naturally occurring curcumin has low bioavailability but light exposure has been shown to improve the bioavailability of curcumin. They investigated that light exposed curcumin increases efficacy in cell lines. TCCSUP, UMUC3, and RT112 cells were preincubated with low concentrations curcumin and then lighted to visible light 1.65 J/cm2. Cell growth, cell proliferation, apoptosis, cell cycle progression were investigated. Cell proliferation, apoptosis, and tumor cell growth were strongly arrested when visible lighted curcumin was used. Light exposed Curcumin caused inhibition in different phases: RT112 in G0/G1 phase, TCCSUP in G2/M phase, and UMUC3 in S-phase. Light exposure on curcumin increases the potential of antitumor on cancer cells.
Mutational analysis of minichromosome maintenance complex component (MCM) family genes in Chinese Han women with polycystic ovarian syndrome
Published in Gynecological Endocrinology, 2023
Jiangyan Zhou, Faying Liu, Lifeng Tian, Ming Yang, Jun Tan, Xianxian Liu, Peishuang Li, Jia Chen, Ge Chen, Lixian Xu, Lisha Peng, Qiongfang Wu, Yang Zou
The minichromosome maintenance (MCM) family is highly conserved in vertebrates and comprises MCM2 through MCM10. These proteins play essential roles in DNA replication and cell cycle progression. Indeed, MCM proteins not only interact with S-phase checkpoint regulators, but also with components of DNA repair pathway [14–16]. The MCM 2-7 complex is instrumental for cell-cycle control, an operation that occurs during the G1 and G2 phases of mitosis [14,15]. MCM8 complexes with MCM9 and has a role in DNA repair and genome instability [17–19]. MCM10 involves in DNA replication and chromosomal instability [16,20]. Recently, studies showed that dysfunctional mutations in MCM8 and MCM9 could lead to premature ovarian failure (POF) and primary ovarian insufficiency (POI) [19,21–23]. Considering the shared biological features between POF/POI and PCOS, such as dysregulation of steroid hormones, and ovarian dysfunction, moreover, some mutations in POF/POI also exist in PCOS, such as AMH, FSHR, GDF9, and BMP15 [24–26], thus, we speculate that mutations/rare variants of MCMs might exist in Chinese patients with PCOS.
Therapeutic efficacy of cyclin-dependent kinase inhibition in combination with ionizing radiation for lung cancer
Published in International Journal of Radiation Biology, 2023
Jenny Ling-Yu Chen, Chun-Kai Pan, Li-Cheng Lin, Ching-Yi Tsai, Ching-Ying Kuo, Yu-Sen Huang, Yu-Li Lin
Cyclin-dependent kinases (CDKs) play critical roles in cell cycle progression in malignant cells (Santo et al. 2015). CDK-dependent pathway deregulation is commonly observed in NSCLC, indicating vulnerabilities that can be exploited for clinical benefit (Sterlacci et al. 2012). CDKs and cyclins are commonly elevated in NSCLC with prognostic implications (Mohamed et al. 2007; Qin et al. 2020). Preclinical evidence has shown that CDK inhibition exerts direct cytotoxicity on lung cancer cells through various mechanisms, including impaired DNA damage repair, dysregulated expression of the centrosomal protein, induced cell cycle arrest and anaphase catastrophe, growth inhibition and apoptosis, suppressed glycolysis, and inhibited proliferation (Galimberti et al. 2010; Hu et al. 2015). CDK inhibition alone in patients with NSCLC is discouraged because it has not demonstrated a significant clinical benefit based on published literature (Le Tourneau et al. 2010; Patnaik et al. 2016; Edelman et al. 2019).
Concanavalin A promotes angiogenesis and proliferation in endothelial cells through the Akt/ERK/Cyclin D1 axis
Published in Pharmaceutical Biology, 2022
Jing-Zhou Li, Xiao-Xia Zhou, Wei-Yin Wu, Hai-Feng Qiang, Guo-Sheng Xiao, Yan Wang, Gang Li
Cell cycle progression plays an essential role in the cell proliferation process. We then explored the effect of Con A on the cell cycle with flow cytometry in HUVECs. Figure 2(G) (HUVECs) and 2H (EA.hy926) showed the representative of the cell cycle distribution with flow cytometry graphs. Figure 2(I,J) illustrate the percentage of cycling progression phases in HUVECs (Figure 2(I)) or EA.hy926 cells (Figure 2(J)) treated with vehicles or different concentrations of Con A. In Con A-treated cells, especially 3 μg/mL, the cells in the G0/G1 phase were significantly decreased, while the cells in S-phase and G2/M phase were increased considerably. These results suggest that Con A-promoted angiogenic effect in HUVECs may mainly be mediated by cell proliferation via promoting the G0/G1 boundary to the S phase.