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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
Pathological Manifestations and Mechanisms of Metal Toxicity
Published in Debasis Bagchi, Manashi Bagchi, Metal Toxicology Handbook, 2020
Cd can also significantly increase the levels of lipid peroxidation in the parietal cortex, striatum, and cerebellum in a mechanism that is related to increased ROS and alteration of mitochondrial function associated with increased levels of COX, activation of MAPK, and mTOR (mammalian target of rapamycin). Additionally, Cd can be transported to the olfactory bulbs by the olfactory neurons causing olfactory dysfunction (B. Wang & Du, 2013; H. Wang, Zhang, Abel, Storm, & Xia, 2018). Once it enters the cell, cytotoxicity can be mediated by inhibition of DNA repair and production of ROS leading to oxidative stress. Intracellular Cd regulates Ca2+ signaling via the 1,4,5-trisphosphate (IP3) pathway and ryanodine, and it increases intracellular Ca2+ concentrations by increased promoting calcium efflux from the endoplasmic reticulum (Branca et al., 2018). Oxidative stress is one of the main components of Cd pathology, with altered glutathione levels and catalase enzyme activity (Menon, Chang, & Kim, 2016). Exposure to Cd, associated with decreased endothelial cell viability, was related to increased production of ROS. This causes a decrease in rat brain phospholipids (PLs) due to the activation of phospholipase A2 enzymes (sPLA2, cPLA2) leading to the release of arachidonic acid, increased COX2 and generation of proinflammatory cytokines including IL1, IL6, TNF-α, iNOS, and interferon gamma (INF-γ). Additionally, increases in pro-apoptotic molecules, such as Bcl-2-associated X protein (Bax), and decreases in anti-apoptosis B-cell lymphoma 2 (Bcl2) were also observed with Cd exposure (Sivaprakasam, Vijayakumar, Arul, & Nachiappan, 2016). The mechanism of Cd-induced neuronal apoptosis has been associated with the Fas/FasL (Fas-Ligand) system involving the mitochondrial apoptotic pathway with increased expression of Fas, Fas-L, Fas-associated death domain (FADD) and cleaved caspase 8 (Yuan et al., 2018).
Effects of zinc on expression of apoptosis-related genes in freezing thawing damage of adipose tissue derived mesenchymal stromal cells
Published in Preparative Biochemistry & Biotechnology, 2022
Fatemeh Nesari, Mohammadreza Gholami, Jafar Rezaian, Afshin Pirnia, Khatereh Anbari, Masoud Beigi Boroujeni, Mandana Beigi Boroujeni
The amount of viability of cells is affected by freezing process.[30] In our study, the percentage of live cells in the control group was about 80% which was supported by other studies.[31] There are two general pathways for apoptosis; intrinsic and extrinsic. Intrinsic pathway—also called as mitochondrial pathway—is associated with mitochondrial proteins such as cytochrome C, Apaf-1 and Bcl2 family proteins. These proteins results in the regulation of Caspase9 and Caspase9, in turn, activates the Caspase3 which is placed at the joining point of the pathways. Extrinsic pathway—also called as death receptor pathway—starts by interaction Fas (death receptor) and Fas ligand (death ligand). This pathway continues to Caspase8 and then Caspase3 as the common point of the pathways.[31,32] Bcl2 family proteins consist of Bak, Bax and Bcl2 placing in mitochondria. Bax is an apoptosis activator resulting in release of cytochrome C while Bcl2 an apoptosis inhibitor.[33,34]
Hesperetin upregulates Fas/FasL expression and potentiates the antitumor effect of 5-fluorouracil in rat model of hepatocellular carcinoma
Published in Egyptian Journal of Basic and Applied Sciences, 2020
Merna G. Aboismaiel, Mohamed El-Mesery, Amro El-Karef, Mamdouh M. El-Shishtawy
Fas (CD95/APO-1) is a type-I trans-membrane protein that belongs to tumor necrosis factor (TNF) receptor superfamily [9]. The extrinsic apoptotic pathway can be initiated through interaction of Fas ligand (FasL) with its corresponding death receptor, Fas. This results in recruitment of the adaptor molecule Fas-associated death domain (FADD) to form a death inducing signaling complex (DISC) with procaspase-8. Cleavage of procaspase-8 results in activation of caspase-8, which mediates activation of downstream caspases and subsequent induction of apoptosis [10]. On the contrary, apoptosis can be suppressed via increased expression of B cell lymphoma-2 (Bcl-2) antiapoptotic proteins causing cancer cells to develop insensitivity toward chemotherapy and thus progression of cancer [11].
Chelidonium majus crude extract induces activation of peripheral blood mononuclear cells and enhances their cytotoxic effect toward HeLa cells
Published in International Journal of Environmental Health Research, 2021
Ana Popovic, Milena Deljanin, Suzana Popovic, Danijela Todorovic, Predrag Djurdjevic, Sanja Matic, Milan Stankovic, Dusko Avramovic, Dejan Baskic
Double positive monocytes (DPMos) that express both CD4 and CD8 can also be detected in peripheral blood of healthy humans (Baba et al. 2006). In myosin-induced myocarditis in rats, Baba et al. (2008) showed a significant increase in the number of DPMos as prevailing infiltrating cells in cardiac lesions. These cells had a high expression of Fas ligand and cytotoxic factors such as perforin and granzyme B and exerted cytotoxic activity against tumor cells. Statistically significant increase in the ratio of monocytes double positive for CD4 and CD8 detected after CME treatment refers to the evolution of activated cells with enhanced cytotoxic potency.