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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
Antitumoral activity of Caralluma europaea on colorectal and prostate cancer cell lines
Published in Journal of Toxicology and Environmental Health, Part A, 2023
Inass Samiry, Aline Pinon, Youness Limami, Samira Rais, Younes Zaid, Mounia Oudghiri, Bertrand Liagre, El Mostafa Mtairag
Cell proliferation was evaluated by MTT assay with concentrations ranging from 50 and 800 µg/ml C. europaea aqueous (Figures 1A and 1C) and 50 to 100 µg/ml methanolic extracts (Figures 1B and 1D) treatment for HT-29, HCT116, PC3 and DU145. In our experimental protocol, the % relative cell viability of treated cells compared to control was noted. Figure 1 demonstrates a decrease in cellular proliferation after 48 hr incubation with different extracts of C. europaea in a concentration-dependent manner in HT-29, HCT116, PC3 and DU145 cells. This reduced cellular proliferation found with the methanolic extract of C. europaea was greater than that noted with the aqueous extract in all 4 cancer cell lines after 48 hr exposure. The methanolic extract of C. europaea presented inhibitory activity in all 4 cell lines with approximately the same IC50 values: HT-29 (IC50 = 73.08 ± 4.46 µg/ml), HCT116 (IC50 = 67.08 ± 0.66 µg/ml), PC3 (IC50 = 63.56 ± 1.58 µg/ml) and DU145 (IC50 = 64.94 ± 0.66 µg/ml) after 48 hr incubation. In contrast, the aqueous extract decreased proliferative activity in only two human colorectal cancer cell lines with IC50 values: 745.93 ± 13.94 µg/ml and 320.96 ± 24.76 µg/ml for HT-29 and HCT116 cells, respectively (Table 1). Based upon these findings, only the methanolic extract of C. europaea was used to investigate mechanisms underlying the observed antiproliferative activity on human colorectal and prostate cancer cells.
Diazinon toxicity in hepatic and spleen mononuclear cells is associated to early induction of oxidative stress
Published in International Journal of Environmental Health Research, 2022
Manuel Iván Girón-Pérez, Verónica S. Mary, Héctor R. Rubinstein, Gladys A. Toledo-Ibarra, Martín G. Theumer
In the present study, it was found that the toxic effects of OPs are not limited to the inhibition of cholinesterase enzymes; it was also found that diazinon may induce early oxidative stress (0.5–4 h), which could contribute to the hepatotoxic and immunotoxic actions of this pesticide. It was observed that in vitro exposure to low-dose diazinon (µM doses) caused an increase in the ROS concentration, both in hepatic and immunological cells. These results coincide with those reported by Deferme et al. (2015), who demonstrated in HepG2 cells that exposure to diazinon (250 μM) for 48 and 72 h caused significant ROS increases. Boussabbeh et al. (2016) also reported that after a 24 h exposure, this pesticide (>300 μM) induced a dose-dependent increase of ROS in HCT116 cells derived from colorectal cancer. In our study, it was observed that free radical accumulation was shown to be an early event, since a significant increase of O2•- level (initial ROS synthesized within the cell) was found after 0.5 h of exposure to diazinon (20–50 μM), and this was maintained at high levels until at least 24 h of culture in both studied cell types. Deferme et al. (2015) suggest that this oxidative stress may occur because diazinon is metabolized by oxidative desulfurization to diazoxon, which may reduce the antioxidant capacities, and this can drastically alter the physiological balance between oxidants and antioxidants, and ultimately can lead to oxidative stress.
Establishment and elicitation of transgenic root culture of Plantago lanceolata and evaluation of its anti-bacterial and cytotoxicity activity
Published in Preparative Biochemistry & Biotechnology, 2021
Samaneh Rahamouz-Haghighi, Khadijeh Bagheri, Ali Sharafi, Hossein Danafar
Therapy effects of apigenin on various cancers including melanoma, osteosarcoma, lung cancer, breast, liver, prostate[89] colorectal cancer cell lines DLD1 and SW480[90] also induction apoptosis HCT116 cells have been studied in numerous investigations.[91] Furthermore, gallic acid exhibited great cytotoxicity effect on cancerous cells, with no inhibition effect on normal cells.[92] Additionally, it was shown that Gallic acid inhibits the proliferation of cholangiocarcinoma cell lines (M213, M214).[84] Another important compound as an anti-cancer agent is catalpol which inhibited Human solid tumor cell lines (A2780, HBL-100, HeLa, SW1573, T-47D and WiDr),[93] Human gastric cancer cells (MKN-45),[94] Human colorectal cancer cells (HCT116),[95] Human non–small-cell, lung cancer (NSCLC) cells- A549 cells[96] and Athymic nude mice.[94]