China
Africa
Explore chapters and articles related to this topic
The Role of Nanoparticles in Cancer Therapy through Apoptosis Induction
Published in Hala Gali-Muhtasib, Racha Chouaib, Nanoparticle Drug Delivery Systems for Cancer Treatment, 2020
Marveh Rahmati, Saeid Amanpour, Hadiseh Mohammadpour
Upon interaction of FasL with Fas receptor (Apo-1 or CD95), the death-inducing signaling complex (DISC), which contains adaptor proteins such as FADD and procaspase-8, is formed. In some cell types, activated CASP-8 directly activates other members of the caspase family and subsequently leads to the execution of apoptosis. In other types of cells, the induction of Fas pathway is not sufficient to trigger an apoptotic response, rather this pathway cross-talk with mitochondrial pathway through proteolytic degradation of Bid producing a truncated form of Bid (tBid). Then, tBid acts through a heterodimer with BAX or BAK, leading to the activation of the mitochondrial pathway of apoptosis. In this situation, the extrinsic pathway functions as an amplifier to induce an apoptotic response [35].
Terpenoids: The Biological Key Molecules
Published in Dijendra Nath Roy, Terpenoids Against Human Diseases, 2019
Moumita Majumdar, Dijendra Nath Roy
Apoptosis or type-1 programmed cell death is initiated by the activation of death receptor (DR) signalling through the binding of the Fas receptor (FasR), TNF receptor (TNFR), DR3, DR4 and DR5 with their respective ligands, resulting in conformational change. After oligomerisation of the receptor via ligands, specialized adaptor proteins activate the caspase cascades. Trimerisation of Fas by binding with FasI recruits adaptor protein Fas-associated death domain (FADD), which activates caspase-8. After oligomerisation, caspase-8 initiates the signalling that stimulates apoptosis via two parallel pathways. In the absence of the caspase cascade, death receptors activate another alternative signalling system designated as necroptosis via formation of the IIb complex. As the largest group of natural products, plant terpenoids have a promising effect on death domain signalling.
The Multiple Facets of Mesenchymal Stem Cells in Modulating Tumor Cells’ Proliferation and Progression
Published in Jince Thomas, Sabu Thomas, Nandakumar Kalarikkal, Jiya Jose, Nanoparticles in Polymer Systems for Biomedical Applications, 2019
Rajesh Ramasamy, Vahid Hosseinpour Sarmadi
Several studies have revealed that MSCs induce cancer proliferation by exploiting the antiapoptotic mechanism within the cancer cells. Apoptosis is a well-regulated mechanism controlled by anti and proapoptotic proteins, could be induced by intracellular or extracellular signals such as first apoptosis signal (FAS) receptor and FAS ligand, TNF-α, caspase, DNA-damaging agents, or mitochondrial activation and p53. In this regard, Castells et al. showed that conditioned medium of MSCs (soluble factor/s) induced an antiapoptotic effect on ovarian cancer cells by preventing the caspases 3 and 7 activity and activating the PI3K/Akt pathway signaling.58 Furthermore, another study found that murine and human MSCs induced the antiapoptotic effect in chronic lymphocytic leukemia via cell-to-cell contact manner by increasing the level of myeloid cell leukemia-1 and poly ADP ribose polymerase protein.59 In addition, Wu et al. demonstrated that MSCs promote colorectal cancer (HCT116 cells) proliferation via decreasing the protein expression level of Bax and p53; apoptosis-related proteins and increasing the protein expression level of antiapoptotic protein, B-cell lymphoma 2 (BCL-2).60
Antitumor activity of solamargine in mouse melanoma model: relevance to clinical safety
Published in Journal of Toxicology and Environmental Health, Part A, 2022
Ricardo Andrade Furtado, Saulo Duarte Ozelin, Natália Helen Ferreira, Bárbara Ayumi Miura, Silvio Almeida Junior, Geórgia Modé Magalhães, Eduardo José Nassar, Mariza Abreu Miranda, Jairo Kenupp Bastos, Denise Crispim Tavares
Yu, Sheu, and Lee (2017) also found that the Solanum incanum extract, rich in solamargine, reduced tumor size in mouse lung tissue associated with apoptosis. Shiu et al. (2007) reported that solamargine was more cytotoxic than other chemotherapeutic agents in breast cancer cells (HBL-100, ZR-75-1, and SK-BR-3). Solamargine induced apoptosis by regulation of tumor necrosis receptor factor (TNFR-1), Fas receptor (Fas), TNFR-1 tumor-associated necrosis receptor factor type DEATH domain protein (TRADD), cytokine and mitochondrial release, as well as activation of caspases 3, 8 and 9 by increasing Bax expression and diminishing Bcl-2 and Bcl-xL expression (Shiu et al. 2007). Thus, significant reduction in mitosis frequencies following solamargine treatment might be partially associated with antiproliferative and apoptotic activities. Further, the B16 murine melanoma cell line is susceptible to induction of apoptosis and cell cycle arrest (Yu, Sheu, and Lee 2017).
Dietary ingestion of 2-aminoanthracene (2AA) and the risk for type-1 diabetes (T1D)
Published in Journal of Environmental Science and Health, Part A, 2020
Isaiah Seise, Zachary A. Pilz, Moses Yeboah Kusi, Bethany Bogan, Brittany Jean McHale, Worlanyo E. Gato
Inflammatory cytokines and apoptosis genes that play various roles in relation to T1D were quantified in the pancreas of all three groups. Upregulation of IL-6, IL-7, and IL-1β in the low and high 2AA concentration groups relative to the control group was observed. It is reasonable to note that the overexpression of these pro-inflammatory proteins was an indication of a more pronounced autoimmune activity in the pancreas. Cells produce small proteins such as cytokines which have peculiar effects on communication and interaction among cells.[17] Cytokines are key intermediaries of inflammation through guiding of innate and adaptive immune responses and tissue damage.[18] Autoimmune disorders such as rheumatoid arthritis and multiple sclerosis have been reported to be associated with overexpression of IL-6.[18] IL-1β secreted by macrophages in the pancreas attract immune cells including dendritic cells and T lymphocytes into the islets which then attack the β-cells.[19] IL-1β can increase the susceptibility of β-cells to apoptosis by raising the production of pro-apoptosis proteins including Fas receptor.[19] Also, IL-7 was overexpressed in the pancreas of rats that ingested 2AA contaminated diets. Recent studies have revealed that homeostatic IL-7 can increase autoreactive T-cell differentiation and expansion.[20] The destruction of β-cells and the pathogenesis of T1D are mediated by T-cells. The upregulation of IL-7 will, therefore, result in an increased presence of T-cells in the pancreas of rats in the treated groups.