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Comparison of Healing Effect of DMSP in Green Sea Algae and Mesenchymal Stem Cells on Various Inflammatory Disorders
Published in Se-Kwon Kim, Marine Biochemistry, 2023
Whereas the pace of population aging around the world is increasing dramatically (WHO, 2015). Aging is the fundamental and unavoidable factor for the development of cancer. The incidence of cancer rises dramatically with age, most likely due to a build-up of risks for specific cancers that increase with age. The overall risk accumulation is combined with the tendency for cellular repair mechanisms to be less effective as a person grows older. Therefore, cancers have been the most tragic and terrible disorders for humans. In the cells of tissues and organs, the cellular senescence is exposed to nonlethal intrinsic or extrinsic stress that results in persistent growth arrest with a distinct morphological and biochemical phenotype. The engagement of senescence may represent a key component for therapeutic intervention in the eradication of cancer occurring with ageing. Normal cells in the body follow an orderly path of growth, division, and death. When this process breaks down, cancer begins to form. Unlikely, regular cells, cancer cells do not experience programmatic death and instead continue to grow and divide. This leads to a mass of abnormal cells that grow out of control. Accordingly, the cellular senescence in anti-cancer therapy may be important also in aging because of the age related-changes down-regulation at the level of both cancer suppressor genes and immune functions (Provinciali et al., 2013; Fulop et al., 2013; Tollefsbol, 2014). This indicates that people age 65 and older bear a higher risk of suffering from cancer compared to younger people (Misra, Seo & Cohen, 2004; WHO, 2018).
Mechanisms of Different Anticancer Drugs
Published in Anjana Pandey, Saumya Srivastava, Recent Advances in Cancer Diagnostics and Therapy, 2022
Anjana Pandey, Saumya Srivastava
The ends of chromosomes are called telomeres, consisting of a repetitive sequence of TTAGGG. The telomerase enzyme adds these specific DNA elements. This enzyme is a ribonucleoprotein complex and responsible for maintaining the length of telomeres in human stem cells and 85% of cancer cells (Shay and Bacchetti, 1997). Another telomere expansion procedure is used in 15% of cancers (Heaphy et al., 2011). During cell division, telomere shortening occurs in normal somatic cells for growth seizure, called cellular senescence. Hence, its long-term stability offers cancer cells infinite proliferation ability and cancer cells can grow indeterminately due to higher telomerase expression (Hanahan and Weinberg, 2011). In this targeting process, a telomere crisis occurs in RB- and p53-deficient cells due to ongoing telomere shortening. This phenomenon can cause different genomic aberrations. Telomerase activation permits cancer cells to escape from disaster and damage genome integrity costs (Maciejowski and deLange, 2017).
Introduction to Cancer, Conventional Therapies, and Bionano-Based Advanced Anticancer Strategies
Published in D. Sakthi Kumar, Aswathy Ravindran Girija, Bionanotechnology in Cancer, 2023
Cellular stress that activates P53 induces apoptosis. During the cell cycle arrest, the weak and sustained activation can promote cell death known as senescence. Cellular senescence is pathophysiological condition by which the cells permanently lose their proliferative capacity. Senescence cell shows specific-morphological features, including flattening, nuclear enlargement, enriched with vacuoles, and altered chromatin structure. In the biochemical level, cellular senescence is characterized by increased ß-galactocidase activity that increases senescence markers, such as P15, P16, P21, P53, and ARF.
Ex vivo treatment with fucoidan of mononuclear cells from SARS-CoV-2 infected patients
Published in International Journal of Environmental Health Research, 2022
K. J. G. Díaz-Resendiz, G. A. Toledo-Ibarra, R. Ruiz-Manzano, D.A. Giron Perez, C.E. Covantes-Rosales, A. B. Benitez-Trinidad, K. M Ramirez-Ibarra, A. T. Hermosillo Escobedo, I. González-Navarro, G.H. Ventura-Ramón, A. Romero Castro, D. Alam Escamilla, A. Y. Bueno-Duran, Manuel Iván Girón-Pérez
Besides, cellular senescence was also evaluated (Figure 3), which plays a beneficial role by preventing tumor development through cell proliferation suppression mechanisms and is associated with tissue regeneration, particularly in epithelial cells and fibroblasts (Lee et al. 2015). Concerning fucoidan, this compound decreased the senescence of mononuclear cells from endothelial colony-forming cells isolated from human umbilical cord blood, indicating that fucoidan rescues these cells from replicative senescence (Lee et al. 2015). As for the immune system, senescence is an aging process often called immunosenescence, that increases cancer, infection, and autoimmune disease susceptibility, especially in older individuals (Prelog 2006; Falci et al. 2013; Pietrobon et al. 2020). In SARS-CoV-2 infected patients, the immunosenescence process appears to play a significant role in COVID-19 prognosis, associated with the increased inflammatory cytokines production during this disease (Pietrobon et al. 2020), thus we evaluate the senescence in immune cells (PBMCs). Obtained results showed that neither the infection nor the treatment with fucoidan exerted an effect on cell senescence on PBMCs from any of the studied groups. However, further tests must be performed to evaluate the association between immunosenescence and the severity of COVID-19 in immune cells, as well as its association with patient age.
Transcriptome alterations in zebrafish gill after exposure to different sizes of microplastics
Published in Journal of Environmental Science and Health, Part A, 2022
Ying-Hao Xue, Tao Jia, Ning Yang, Zhan-Xiang Sun, Zhi-Yu Xu, Xin-Li Wen, Liang-Shan Feng
After exposure to 90-106 μm and 250-300 μm MPs, four important KEGG pathways were significantly regulated. Among them, cellular senescence is generally defined as a stable cell cycle arrest in response to diverse stressors, including replicative exhaustion, DNA damaging agents, oncogene activation, mitochondrial deterioration, and oxidative stress (Figure 6).[41] The FOXO signaling pathway is involved in the cell cycle, apoptosis, autophagy regulation, oxidative stress resistance, immune regulation, and glycolysis/gluconeogenesis (Figure 7).[42] The p53 signaling pathway regulates a wide variety of cellular processes including cell cycle arrest, apoptosis, oxidative stress resistance, DNA repair and damage prevention (Figure 8).[43,44] These three pathways closely connect to each other. Enrichment of these three pathways suggested that 90-106 μm and 250-300 μm MPs exposure might influence one or more of the following functions: cell cycle, cell damage, apoptosis, and oxidative/antioxidant responses. Notably, cdkn1a (p21), ccnd2, gadd45 (gadd45aa, gadd45bb, gadd45ga), and ptenb were the four key hub genes in these pathways, deserving further investigations.
Air pollution and molecular changes in age-related diseases
Published in International Journal of Environmental Health Research, 2022
B. Hermanova, P. Riedlova, A. Dalecka, V. Jirik, V. Janout, R. J. Sram
Telomeres are the end parts of eukaryotic chromosomes, which protect their stability and the overall integrity of DNA against loss of genetic information (Blackburn 1991). During a life, i.e. as the number of cell divisions increases, these telomeres gradually get shorter. Therefore, telomere length tends to be referred to as a marker of cell aging or cellular ‘senescence’ (Levy et al. 1992; Robin et al. 2014; Bernadotte et al. 2016). Changes in telomere lengths and related telomerase activity may be affected by oxidative stress and inflammatory processes induced by environmental factors (Von Zglinicki 2002).