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Marine Algal Secondary Metabolites Are a Potential Pharmaceutical Resource for Human Society Developments
Published in Se-Kwon Kim, Marine Biochemistry, 2023
Somasundaram Ambiga, Raja Suja Pandian, Lazarus Vijune Lawrence, Arjun Pandian, Ramu Arun Kumar, Bakrudeen Ali Ahmed Abdul
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).
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.
The N-Myc Oncogene in Pediatric Tumors: Diagnostic, Prognostic and Biological Aspects
Published in John T. Kemshead, Pediatric Tumors: Immunological and Molecular Markers, 2020
In view of their postulated role in tumor pathogenesis, the biochemical functions of protooncogenes in the normal cell are of considerable interest. Many findings now indicate that the protein products of c-oncs are fundamentally involved in information pathways between the surface membrane and the nucleus. These regulate the key functions of cell growth, division, and differentiation. The oncogene products so far analyzed (see Table 1) fall into five groups:2,13 (1) proteins homologous to growth factors, e.g., c-sis, which codes for the beta chain of platelet derived growth factor;14 (2) membrane bound proteins possessing tyrosine kinase activity and related to growth factor receptors, e.g., v-erb B, which codes for a truncated form of the epidermal growth factor receptor;15 (3) cytoplasmic proteins with serine kinase activity, e.g., the products of c-raf and c-mos; (4) membrane bound proteins with GTPase activity, possibly mediating interactions between cell surface receptors and effector enzyme systems, e.g., the p21 c-ras protein; and (5) proteins located in the cell nucleus, e.g., the products of c-myb, c-fos, and the myc gene family16 (c-myc, N-myc and L-myc). The biological functions of this last and most enigmatic group, the nuclear oncoproteins, will be discussed further in a later section.
Recent and Evolving Therapies in the Management of Endothelial Diseases
Published in Seminars in Ophthalmology, 2023
Shalini Singh, Sunita Chaurasia
Corneal endothelial cells have the capacity to expand in vitro, but ability to do so in vivo is limited. The first reported protocol for in vitro expansion of endothelial cells was in 1965, and ever since there have been a plethora of protocols explaining isolation and in vitro expansion of endothelial cells because it is extremely challenging to isolate and expand endothelial cells in vitro. Culture and expansion of endothelial cells are achieved by collectively tweaking the following steps: selection of suitable donor tissue, peeling of the corneal endothelium and DM from donor corneas, enzymatic digestion to isolate the hCEC, seeding of the resulting cell suspension using a combination of culture media and growth factors, and expansion and proliferation on appropriate substrates that mimic the in vivo conditions.9 Cell growth is also boosted by the loss of cell contact, supplemented culture medium and growth factors.43 Endothelial to mesenchymal transition is induced by the activation of intra-cellular pathways which causes the CEC to acquire a fibroblast-like phenotype, thereby losing their morphological features and function.43–45Hence, a protocol to achieve isolation, expansion and propagation of CEC along with maintaining cell morphology and function needs to be developed.
Nisin and nisin-loaded nanoparticles: a cytotoxicity investigation
Published in Drug Development and Industrial Pharmacy, 2022
Tanweer Haider, Vikas Pandey, Chittaranjan Behera, Pradeep Kumar, Prem N. Gupta, Vandana Soni
Cancer is a complex disease associated with the uncontrolled growth and proliferation of cells. Despite advances in its detection and treatment, cancer remains a leading cause of death, accounting for approximately 10 million deaths in 2020 [1]. Some of the key factors involved in the development of cancer are escaped by various mechanisms of regulation of cell growth, adaptive behavior, metastasis, etc. The specific and defined mechanisms are available to balance cells' renewal and death in normal cellular conditions. However, abnormalities in cell growth mechanisms cause abnormal cell growth, which leads to changes such as proliferative signaling, growth suppressors escape, resistance to cell death/apoptosis, replicative immortality, excessive angiogenesis, and triggering invasion and metastasis [2]. Several strategies are available for cancer treatment, including chemotherapy, surgery, radiation, etc. In these strategies, chemotherapy is preferably used for cancer treatment, but it has limitations, such as nonspecific drug delivery and toxicity toward normal cells [3]. In such conditions, nanoparticles and targeted drug delivery system overcome the drawbacks of conventional chemotherapy.
Coffee Intake Interacted with the Bcl-2 rs1944420, rs7236090, and rs2849382 Haplotype to Influence Breast Cancer Risk in Middle-Aged Women
Published in Nutrition and Cancer, 2022
Meiling Liu, Sang Shin Song, Sunmin Park
Disruption of the homeostatic balance between cell growth and death plays a crucial role in cancer development. In particular, the over-expressions of antiapoptotic genes and under-expressions of pro-apoptotic genes reduce cell death and may lead to cancer development (25). Organ structure and function are sustained by the regulation of apoptosis by caspases. The Bcl-2 family is composed of subclasses of anti-apoptotic (Bcl-2, Bcl-2-Al, Bcl-XL, Bcl-W, and Mcl-1) and pro-apoptotic caspases (Bad, Bik, Bim, Bak, Bax, Bid, Hrk, Noxa, and Puma). Bcl-2 family proteins interact to regulate cell death decisions by integrating signals and meticulous control of cell growth and death required to produce breast tissues. Bcl-2 protein plays a fundamental role in this process, and its dysregulation suppresses cell death and increases cancer risk (26–28). Bcl-2 overexpression has been reported in a variety of tumors and lymphomas in animal models (29), which suggests Bcl-2 acts as an oncogene. Our findings suggest minor alleles of Bcl-2 dysregulate cell death by stimulating the antiapoptotic function of Bcl-2 and that minor alleles of Bcl-2 are associated with breast cancer.