Marine Algal Secondary Metabolites Are a Potential Pharmaceutical Resource for Human Society Developments
Se-Kwon Kim in Marine Biochemistry, 2023
Cell proliferation is the process in which the number of cells increases due to cell division and cell growth, which often occurs in tumors or cancers. Evidence suggests that algae may act as an antiproliferative by inducing maturation of dendritic cells, combining with other cytokines, and modulating the human immune system (Lowenthal and Fitton, 2015). Macrophages are activated by membrane receptors specifically TLR4, CD14, CR3 and SR, leading to the production of cytokines such as IL-12 and IFN, which enhance the activation of NK cells, which in turn stimulates the activation of T cells (Kellogg et al., 2015). In addition, secondary metabolites of algae, such as root bark tannins, flavonoids, catechins, carotenoids, quercetin, and myricetin, have been shown to have relative anticancer activity. Epidemiological studies also show that, compared to other parts of the world, eating seaweed can reduce the incidence of ovarian cancer, breast cancer, and endometrial cancer in the Japanese population (Murata and Nakazoe, 2001).
Transforming Growth Factor-α and Epidermal Growth Factor
Jason Kelley in Cytokines of the Lung, 2022
Characterization of the EGF family of growth factors and their receptor has generated a great deal of interest in the role they may play in lung development. When considering these growth factors as potential morphogens, it is important to emphasize three features. First, these growth factors are capable not only of inducing cell proliferation, but also of modulating cell differentiation, migration, and metabolism. Second, their transmembrane precursor species can potentially function in cell-cell interactions as adhesion molecules to which cells expressing the EGF receptor can attach. Third, since EGF and TGF-α are biologically active as transmembrane molecules, they can exert a very localized paracrine influence that is limited to contiguous cells. However, if the membrane-associated precursor is proteolytically processed to the mature molecule, then the growth factor is diffusible and capable of influencing more remote cells.
General Surgery
Tjun Tang, Elizabeth O'Riordan, Stewart Walsh in Cracking the Intercollegiate General Surgery FRCS Viva, 2020
What are the limitations of chemotherapy?Cell proliferation mechanisms affect normally dividing and cancer cells.Selectivity towards cancer cells is seen as some tumours are highly proliferative compared with normal cells (e.g. lymphoma) or defective in their ability to repair DNA and therefore cannot repopulateTherapeutic ratio (toxic dose and therapeutic dose) for a drug should be close to 1, so that damage to normal tissues is self-limiting.Drug-induced damage to normal tissue that is rapidly dividing (bone marrow, GI mucosa) can be life threatening.
Synthesis and biological evaluation of halogenated phenoxychalcones and their corresponding pyrazolines as cytotoxic agents in human breast cancer
Published in Journal of Enzyme Inhibition and Medicinal Chemistry, 2022
Peter A. Halim, Rasha A. Hassan, Khaled O. Mohamed, Soha O. Hassanin, Mona G. Khalil, Amr M. Abdou, Eman O. Osman
Anticancer agents exert their cytotoxic action by terminating cellular proliferation at definite checkpoints found at different stages of the cell cycle. Suppression of these phases results in the termination of the cell proliferation. Cell cycle analysis employs flow cytometry to differentiate between cells within different phases of the cell cycle. In this work, the effect of the most active compound 2c on cell cycle progression was studied to explore the definite phase at which cell cycle arrest takes place in the MCF-7 breast cancer cell line. MCF-7 cells were treated with compound 2c at its IC50 concentration (1.52 μM) and its effect on the cell population in different cell phases was recorded and displayed in Figure 5. Exposure of MCF-7 cells to compound 2c resulted in significant decline in the cell population at the G0/G1 and S phases with 54.73% (from 55.05% to 24.92%) and 14.5% (from 34.18% to 29.22%), respectively. Moreover, marked augmentation was observed in the proportion of cells in the G2/M phase by 4.25-fold, and in the pre-G1 phase by 16.24-fold, in comparison to the control (DMSO). This clearly indicates that the target chalcone derivative 2c arrested the cell cycle proliferation of MCF-7 cells in the G2/M phase.
Application in Gene Editing in Ovarian Cancer Therapy
Published in Cancer Investigation, 2022
Shuang Luo, Yujiao Wang, Yongyu Tao, Shuo Li, Zirui Wang, Wei He, Hangxing Wang, Nan Wang, Jianwei Xu, Hailiang Song
Yahata et al. found that the proportions of CD4+ T cells, CD8+ T cells, and CD49+ NK cells were significantly increased by inhibition of PD-L1 expression in a mouse model of OC with ID8 cells and inhibited the progression of intraperitoneal tumors (30). Therefore, it can be concluded that PD-L1 is related to the production of immune cells, which in turn control the spread of tumors. In addition to inhibiting the occurrence of tumors by controlling the proliferation of cells, tumor cell proliferation can also be inhibited by increasing drug sensitivity. On this basis, de Groote ML et al. found that cisplatin is less sensitive to ATF-induced ICAM-1 (intercellular adhesion molecule 1) positive ovarian cancer cells, but gene editing specifically induced ICAM-1 expression can inhibit the growth of ovarian cancer cells (31). Therefore, knockout or knockdown of BMI, EPHA1, and PD-L1 and increased expression of ICAM-1 by ATF through CRISPR-Cas9 can delay the proliferation, invasion, migration, and diffusion of tumor cells so as to control the occurrence and development of OC and improve the cure rate (Figure 1).
Liposomal delivery of vascular endothelial growth factor/receptors and their inhibitors
Published in Journal of Drug Targeting, 2020
Farnaz Khodabakhsh, Serge Muyldermans, Mahdi Behdani, Fatemeh Kazemi-Lomedasht
Cancer is currently a major worldwide problem leading to thousands of deaths, every year. One of the key hallmarks of cancer is angiogenesis [1]. Angiogenesis is the formation of new blood vessels from the pre-existing vascular network. It is a multi-step process involving endothelial cell proliferation, migration and tubular structure formation of cells that eventually develop tubular assemblies into vessels. Such blood vessel formations are essential for the growth and dissemination of a solid tumour. Thus, angiogenesis takes a central role in biological processes, both, in physiological conditions and in some pathological conditions including solid cancers [2–4]. Several growth factors are implicated in tumour angiogenesis, of which the most important are those from the family of vascular endothelial growth factors (VEGF) [2].
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