scholarly journals Genotoxicity and oxidative stress induction by polystyrene nanoparticles in the colorectal cancer cell line HCT116

PLoS ONE ◽  
2021 ◽  
Vol 16 (7) ◽  
pp. e0255120
Author(s):  
Giulia Vecchiotti ◽  
Sabrina Colafarina ◽  
Massimo Aloisi ◽  
Osvaldo Zarivi ◽  
Piero Di Carlo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Line ◽  
Hct116 Cell ◽  
Cancer Cell Line ◽  
Colorectal Cancer Cell Line ◽  
Ros Production ◽  
Polystyrene Nanoparticles ◽  
Contaminated Food ◽  
Potential Damage ◽  
The Impact

The potential risks of environmental nanoparticles (NPs), in particular Polystyrene Nanoparticles (PNPs), is an emerging problem; specifically, the interaction of PNPs with intestinal cells has not been characterized so far. The mechanism by which polystyrene particles are transferred to humans has not yet been clarified, whether directly through ingestion from contaminated food. We evaluated the interaction between PNPs and colorectal adenocarcinoma cells (HCT116). Cells were exposed to different concentrations of PNPs, metabolic activity and the consequent cytotoxic potential were assessed through viability test; we evaluated the PNP genotoxic potential through the Cytokinesis-Block Micronucleus cytome (CBMN cyt) assay. Finally, we detected Reactive Oxygen Species (ROS) production after NPs exposure and performed Western Blot analysis to analyze the enzymes (SOD1, SOD2, Catalase, Glutathione Peroxidase) involved in the cell detoxification process that comes into play during the cell-PNPs interaction. This work analyzes the cyto and genotoxicity of PNPs in the colorectal HCT116 cell line, in particular the potential damage from oxidative stress produced by PNPs inside the cells related to the consequent nuclear damage. Our results show moderate toxicity of PNPs both in terms of ROS production and DNA damage. Further studies will be needed on different cell lines to have a more complete picture of the impact of environmental pollution on human health in terms of PNPs cytotoxicity and genotoxicity.

Novel Fluorine Boron Hybrid Complex as Potential Antiproliferative Drugs on Colorectal Cancer Cell Line

2019 ◽  
Vol 19 (5) ◽  
pp. 627-637 ◽  
Author(s):  
Yasin Tülüce ◽  
Hawro D.I. Masseh ◽  
İsmail Koyuncu ◽  
Ahmet Kiliç ◽  
Mustafa Durgun ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Line ◽  
Cancer Cell Line ◽  
Total Antioxidant Status ◽  
Stress Index ◽  
Colorectal Cancer Cell Line ◽  
Hybrid Complex ◽  
Total Antioxidant ◽  
The Impact ◽  
Ht 29

Objective: Colorectal Cancer (CRC) is one of the most common types of cancer in both sexes; it is considered to be the third leading death factor among other types of cancer. : This study aimed to examine the cytotoxicity of a new fluorine boron hybrid complex [L(BF2)2] on human colorectal adenocarcinoma cell line (HT-29), based on the potency of the half-metal based complexes to initiate apoptosis. Methods: Methods: Based on this data, the impact of it in different concentrations on HT-29 cancerous cells was determined by apoptosis (ELISA, DNA fragmentation laddering, AO/EB staining), cytotoxicity (MTT) and genotoxicity (comet assay). We also calculated the cellular Oxidative Stress Index (OSI) by measuring the Total Antioxidant Status (TAS) and Total Oxidant Status (TOS). Results: Firstly, [L(BF2)2] was examined in view of cytotoxic effect in seven various cell lines (HELA, DU-145, PC3, DLD-1, ECC, PNT1-A and HT-29), and then it was found that the applied complex had a mighty antiproliferative action on HT-29 cells. Thus, the most effective IC50 value turned out to be 26.49 µM in HT-29 cell line. The present study found a tremendous efficacy of [L(BF2)2] on HT-29 cells, especially in terms of damage to cancer cells' DNA, and consequently caused a series of reactions leading to programmed cell death. Conclusion: The results suggest that the [L(BF2)2] as a novel fluorine boron hybrid complex can induce the apoptosis of HT-29 colorectal cancerous cell line and is a possible candidate for future cancer studies.

Lopinavir/Ritonavir Treatment Induces Oxidative Stress and Caspaseindependent Apoptosis in Human Glioblastoma U-87 MG Cell Line

2018 ◽  
Vol 16 (2) ◽  
pp. 106-112 ◽  
Author(s):  
Rossella Gratton ◽  
Paola Maura Tricarico ◽  
Rafael Lima Guimaraes ◽  
Fulvio Celsi ◽  
Sergio Crovella
Keyword(s):  
Oxidative Stress ◽  
Flow Cytometry ◽  
Cell Death ◽  
Side Effects ◽  
Cell Line ◽  
Apoptotic Cell ◽  
Mitochondrial Morphology ◽  
Ros Production ◽  
Human Glioblastoma ◽  
The Impact

Background:Lopinavir and Ritonavir (LPV/r) treatment is widely used to prevent HIV mother-to-child transmission. Nevertheless, studies related to the impact of these compounds on patients, in particular in the foetus and newborns, are strictly required due to the controversial findings reported in the literature concerning possible neurologic side effects following the administration of these drugs.Objectives:In our study, we evaluated the impact of LPV/r treatment on the human glioblastoma U- 87 MG cell line.Methods:In order to evaluate the influence of Lopinavir and Ritonavir in terms of oxidative stress (ROS production), mitochondrial morphology and apoptotic cell death, the latter either in the presence or in the absence of caspase-3 and -9 inhibitors, we treated U-87 MG with increasing doses (0.1-1-10-25-50 µM) of Lopinavir and Ritonavir for 24h, either in single formulation or in combination. ROS production was measured by flow cytometry using H2DCFDA dye, mitochondrial morphology was evaluated using MitoRed dye and apoptotic cell death was monitored by flow cytometry using Annexin V-FITC and Propidium Iodide.Results:We observed that co-treatment with Lopinavir and Ritonavir (25 and 50 µM) promoted a significant increase in ROS production, caused mitochondrial network damage and induced apoptosis in a caspase-independent manner.Conclusion:Based on our findings, concordant with others reported in the literature, we hypothesize that LPV/r treatment could not be entirely free from side effects, being aware of the need of validation in in vivo models, necessary to confirm our results.

Synthesis, Cytotoxicity and Antioxidant Activity of New Analogs of RC-121 Synthetic Derivatives of Somatostatin

2019 ◽  
Vol 18 (10) ◽  
pp. 1417-1424 ◽  
Author(s):  
Emilia Naydenova ◽  
Diana Wesselinova ◽  
Svetlana Staykova ◽  
Ivan Goshev ◽  
Ljubomir Vezenkov
Keyword(s):  
Antioxidant Activity ◽  
Antioxidant Capacity ◽  
Cell Line ◽  
Cancer Cell ◽  
Cancer Cell Line ◽  
Colorectal Cancer Cell Line ◽  
Cervical Cancer Cell Line ◽  
Synthetic Derivatives ◽  
Derivatives Of

Background: Based on the structure of RC-121 (D-Phe-c (Cys-Tyr-D-Trp-Lys-Val-Cys)-Thr-NH2, - synthetic derivatives of somatostatin), some analogs were synthesized and tested for in vitro cytotoxic and antioxidant activity. Objectives: The new analogs were modifyed at position 5 with Dap (diaminopropanoic acid), Dab (diaminobutanoic acid) and Orn and at position 6 with the unnatural amino acids Tle (t-leucine). Methods: The in vitro cytotoxic effects of the substances were investigated against a panel of human tumor cell lines HT-29 (Human Colorectal Cancer Cell Line), MDA-MB-23 (Human Breast Cancer Cell Line), Hep G-2 (Human Hepatocellular Carcinoma Cell Line) and HeLa (cervical cancer cell line). The antioxidant capacities were tested by ORAC (Oxygen Radical Antioxidant Capacity) and HORAC (Hydroxyl Radical Averting Capacity) methods. Results: All substances expressed significantly higher antioxidant capacity by comparison with galic acid and Trolox. All substances showed considerable antioxidant capacity as well. Compound 2T (D-Phe-c(Cys-Tyr-DTrp- Dap-Tle-Cys)-Thr-NH2)had the highest antioxidant effect. The compound 4T (D-Phe-c(Cys-Tyr-D-Trp- Orn-Tle-Cys)-Thr-NH2) displayed antiproliferative effect on HeLa cells with IC50 30 µM. The peptide analog 3T (D-Phe-c(Cys-Tyr-D-Trp-Lys-Tle-Cys)-Thr-NH2) exerted the most pronounced inhibition on the cell vitality up to 53%, 56% and 65% resp. against MDA-MB-23, Hep G-2, HeLa in the higher tested concentration. Conclusion: The somatostatin analogs showed moderate influence on the vitality of different tumor cells and could be used in changing their pathology.

scholarly journals 3DIV update for 2021: a comprehensive resource of 3D genome and 3D cancer genome

2020 ◽  
Vol 49 (D1) ◽  
pp. D38-D46
Author(s):  
Kyukwang Kim ◽  
Insu Jang ◽  
Mooyoung Kim ◽  
Jinhyuk Choi ◽  
Min-Seo Kim ◽  
...  
Keyword(s):  
Cell Line ◽  
Large Scale ◽  
Three Dimensional ◽  
Cancer Cell Line ◽  
Cancer Genome ◽  
Structural Variations ◽  
3D Genome ◽  
Tightly Coupled ◽  
Regulatory Effects ◽  
The Impact

Abstract Three-dimensional (3D) genome organization is tightly coupled with gene regulation in various biological processes and diseases. In cancer, various types of large-scale genomic rearrangements can disrupt the 3D genome, leading to oncogenic gene expression. However, unraveling the pathogenicity of the 3D cancer genome remains a challenge since closer examinations have been greatly limited due to the lack of appropriate tools specialized for disorganized higher-order chromatin structure. Here, we updated a 3D-genome Interaction Viewer and database named 3DIV by uniformly processing ∼230 billion raw Hi-C reads to expand our contents to the 3D cancer genome. The updates of 3DIV are listed as follows: (i) the collection of 401 samples including 220 cancer cell line/tumor Hi-C data, 153 normal cell line/tissue Hi-C data, and 28 promoter capture Hi-C data, (ii) the live interactive manipulation of the 3D cancer genome to simulate the impact of structural variations and (iii) the reconstruction of Hi-C contact maps by user-defined chromosome order to investigate the 3D genome of the complex genomic rearrangement. In summary, the updated 3DIV will be the most comprehensive resource to explore the gene regulatory effects of both the normal and cancer 3D genome. ‘3DIV’ is freely available at http://3div.kr.

scholarly journals Seeding of breast cancer cell line (MDA-MB-231LUC+) to the mandible induces overexpression of substance P and CGRP throughout the trigeminal ganglion and widespread peripheral sensory neuropathy throughout all three of its divisions

2021 ◽  
Vol 17 ◽  
pp. 174480692110240
Author(s):  
Silvia Gutierrez ◽  
James C Eisenach ◽  
M Danilo Boada
Keyword(s):  
Breast Cancer ◽  
Substance P ◽  
Cancer Cells ◽  
Cell Line ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Trigeminal Ganglion ◽  
Breast Cancer Cell Line ◽  
Cancer Cell Line ◽  
The Impact

Some types of cancer are commonly associated with intense pain even at the early stages of the disease. The mandible is particularly vulnerable to metastasis from breast cancer, and this process has been studied using a bioluminescent human breast cancer cell line (MDA-MB-231LUC+). Using this cell line and anatomic and neurophysiologic methods in the trigeminal ganglion (TG), we examined the impact of cancer seeding in the mandible on behavioral evidence of hypersensitivity and on trigeminal sensory neurons. Growth of cancer cells seeded to the mandible after arterial injection of the breast cancer cell line in Foxn1 animals (allogeneic model) induced behavioral hypersensitivity to mechanical stimulation of the whisker pad and desensitization of tactile and sensitization of nociceptive mechanically sensitive afferents. These changes were not restricted to the site of metastasis but extended to sensory afferents in all three divisions of the TG, accompanied by widespread overexpression of substance P and CGRP in neurons through the ganglion. Subcutaneous injection of supernatant from the MDA-MB-231LUC+ cell culture in normal animals mimicked some of the changes in mechanically responsive afferents observed with mandibular metastasis. We conclude that released products from these cancer cells in the mandible are critical for the development of cancer-induced pain and that the overall response of the system greatly surpasses these local effects, consistent with the widespread distribution of pain in patients. The mechanisms of neuronal plasticity likely occur in the TG itself and are not restricted to afferents exposed to the metastatic cancer microenvironment.

Sign in / Sign up

Export Citation Format

Share Document