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Urological Anti-cancer Agents
Published in Karl H. Pang, Nadir I. Osman, James W.F. Catto, Christopher R. Chapple, Basic Urological Sciences, 2021
Bernadett Szabados, Thomas Powles
Interphase = cell growth.G1 phase (Post mitotic gap phase). The cell growth begins after mitosis, with the production of cytoplasm and extra organelles.S phase = DNA replication.G2 phase = preparation for mitosis; production of microtubules.M Phase (Mitotic phase) = active cell division.
Small-Molecule Targeted Therapies
Published in David E. Thurston, Ilona Pysz, Chemistry and Pharmacology of Anticancer Drugs, 2021
Although the various stages of interphase are not usually distinguishable from a morphological perspective, each phase of the cell cycle has a set of distinct biochemical processes that prepare the cell for division. Many of the relevant genes were first identified by studying yeast, especially Saccharomyces cerevisiae. The CDK4/6 and CDK2 kinases are required for progression through G1 of the cell cycle and entry into S-phase, and control of these kinases occurs at multiple levels. The first level involves accumulation of the cyclin, the second is assembly into a cyclin-CDK complex, and the third is specific phosphorylation and dephosphorylation events. Additional regulation of G1 CDK activity is mediated by association with inhibitory proteins, the CKIs, that can physically block activation or block substrate/ATP access. The known CKIs are grouped into two gene families, Ink4 and Cip/Kip, according to their structural similarities. The D-type cyclins and their corresponding partner kinases CDK4 and CDK6 act as central integrators of extracellular signals and operate during the G1 phase of the cell cycle by phosphorylating the tumor-suppressor protein pRb, thus contributing to its inactivation. Mutations that can influence the function of cyclins CDK4 and CDK6, their regulating proteins, or pRB, can be found in most human tumors. Furthermore, cyclin D1 expression can be up-regulated by the Ras signaling pathway, which is itself up-regulated in many cancer cell types.
The Fight Against Cancer
Published in Nathan Keighley, Miraculous Medicines and the Chemistry of Drug Design, 2020
Cells undergo a regular cycle of cell division, which is split into three periods. Interphase comprises the majority of the cell cycle, when there is no division, and is subdivided into a further three parts: first growth phase (G1), where organelles produce proteins, synthesis phase, when DNA is replicated, and second growth phase (G2), when organelles grow and divide and energy stores are increased. The second phase is nuclear division, where the nucleus divides into either two (mitosis) or four (meiosis). The last phase is cell division to produce the daughter cells. For mammals, the cell cycle takes about 24 hours, 90% of which is interphase. Most cancers are caused by damage to the genes that regulate mitosis and the cell cycle.
Design, synthesis, docking, and anticancer evaluations of new thiazolo[3,2-a] pyrimidines as topoisomerase II inhibitors
Published in Journal of Enzyme Inhibition and Medicinal Chemistry, 2023
Mona S. El-Zoghbi, Samiha A. El-Sebaey, Hanan A. AL-Ghulikah, Eman A. Sobh
The cell cycle is required for cell division and replication. The cell cycle was divided into four distinct phases: G1 phase (synthesis), S phase (synthesis), G2 phase (interphase), and M phase (mitosis). The G1 phase, also known as the post-mitotic pre-synthesis phase, is distinguished by direct cell division. DNA replication identifies the S phase. The G2 phase, premitotic, or post-synthetic phase, which can be considered the actual division, is when the cell prepares to split into two cells. Finally, the doubled DNA organised in chromosomes is separated during the M- or mitosis-phase division25. Many anticancer drugs cause apoptosis, cell cycle arrest, or a combination of both as part of their cytotoxic action52. As a result, it was worth investigating whether cell cycle arrest was involved in the cytotoxicity mechanism of the most active cytotoxic agent 4c on A549 cells using flow cytometry analysis, and the results were demonstrated in Table 4 and Figure 7. The results revealed a 69.07% increase in cell count at the G0-G1 phase, compared to 56.39% for control cells. While the percentage of cells in the S phase was reduced by 26.89% compared to the control (29.64%). On the other hand, a dramatic fall in the cell population in the G2/M phase was observed upon treatment with compound 4c from 13.97 to 4.04%. As a result, compound 4c was demonstrated to significantly disrupt the cell cycle profile and cause cell cycle arrest.
COVID-19: a wreak havoc across the globe
Published in Archives of Physiology and Biochemistry, 2023
Heena Rehman, Md Iftekhar Ahmad
The N protein has two separate domains, namely the N terminal domain and C terminal domain. The N protein in different viruses uses different mechanisms for binding to the RNA. The N terminal domain is heavily phosphorylated. It binds to the viral genome in beads on a string manner. There are basically two substrates of N protein. One of the substrates is the trinucleotide repeat sequence (TRSs) which binds to the C terminus and other substrate binds to the genomic packaging signal. The gene coding for N protein precedes the 3′UTR of the coronavirus genome (Rota et al.2003). Nucleocapsid is involved in viral packaging, viral core formation, and vRNA synthesis (Hiscox et al.2001). The N protein of novel coronavirus consist of a short lysine rich region (KTFPPTEPKKDKKKKTDEAQ) near the C terminal which is unique (Marra et al. 2003). It is speculated that this region acts as a nuclear localising region which allows N protein to enter the nucleus through passive diffusion (Rowland et al.1999). It gets phosphorylated after translation. The phosphorylation allows it to enter the nucleus at specific stages of the cell cycle (Hiscox et al.2001). During the interphase, the N protein gets an opportunity to interact with various transcription factors and regulatory complexes. N protein affects the signal transduction pathways resulting in inflammation, apoptosis, and several other cellular processes.
Low dose gamma irradiation pretreatment modulates the sensitivity of CNS to subsequent mixed gamma and neutron irradiation of the mouse head
Published in International Journal of Radiation Biology, 2021
Alla V. Rodina, Yulia P. Semochkina, Olga V. Vysotskaya, Anastasia N. Romantsova, Aleksandr N. Strepetov, Elizaveta Y. Moskaleva
The procedure was carried out in accordance with the method of Legroux et al. (2015). After the perfusion, the brains were extracted from the skull and the cerebellum and olfactory lobes were removed. The brains from each mouse were placed in cold PBS with sucrose (20 g/L) and glucose (0.9 g/L) and kept on ice at +4 °C. Then the PBS was decanted, the brain was thoroughly chopped with a scalpel in StemPro™ Accutase™ Cell Dissociation Reagent (ThermoFisher Scientific, USA), transferred to a test tube, another 2 mL of accutase was added and incubated in a water bath at +37оС for 15 min with stirring. Afterward, 10% by volume of fetal bovine serum was added to the specimens, which were placed in an ice bath. The tissue homogenate was rubbed through a nylon mesh with a pore size of 100 µm. Centrifuged cells were suspended in 20% Percoll (GE Healthcare, USA) (10 mL per 1 brain). Percoll was layered with Hanks solution and centrifuged. Myelin was present in interphase, while cells were sedimented to the bottom. The myelin layer and supernatant were removed. The cell pellet was washed 2 times with PBS. The cell number was counted in the Goryaev,s chamber.