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Specialty: Cancer & Oncology
Drug: Acetylcysteine

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Total 16 results found since Jan 2013.

The role of the Nrf2/GSH antioxidant system in cisplatin resistance in malignant rhabdoid tumours
ConclusionsThese results suggest that targeting the Nrf2/GSH antioxidant system may present a novel therapeutic strategy to combat chemoresistance in rhabdoid tumours.
Source: Journal of Cancer Research and Clinical Oncology - July 28, 2023 Category: Cancer & Oncology Source Type: research

Synthesis and anti-melanoma effect of 3-O-prenyl glycyrrhetinic acid against B16F10 cells via induction of endoplasmic reticulum stress-mediated autophagy through ERK/AKT signaling pathway
In this study, 4-phenylbutyric acid (4PBA, a chemical chaperone) and small interference RNA (siRNA) knockdown of C/EBP Homologous Protein (CHOP)/growth arrest- and DNA damage-inducible gene 153(GAD153) blocked NPC-402-mediated autophagy induction, thus confirming the role of ER stress and autophagy in melanoma cell death. NPC-402 induced oxidative stress and apoptosis in melanoma cells, which were effectively mitigated by treatment with N-acetylcysteine (NAC). In vivo studies showed that intraperitoneal (i.p.) injection of NPC-402 at 10 mg/kg (5 days in 1 week) significantly retarded angiogenesis in the Matrigel plug assay...
Source: Frontiers in Oncology - August 2, 2022 Category: Cancer & Oncology Source Type: research

Downregulation of MUTYH contributes to cisplatin ‑resistance of esophageal squamous cell carcinoma cells by promoting Twist‑mediated EMT.
In conclusion, the present data demonstrated that EMT activation mediated by MUTYH downregulation, by both enhancing Twist transcription and blocking its degradation, is one of the mechanisms for acquisition of CDDP resistance in ESCC. PMID: 31578574 [PubMed - as supplied by publisher]
Source: Oncology Reports - October 4, 2019 Category: Cancer & Oncology Tags: Oncol Rep Source Type: research

Sanguinarine Induces Apoptosis Pathway in Multiple Myeloma Cell Lines via Inhibition of the JaK2/STAT3 Signaling
In this study, we aimed to investigate the potential anti-proliferative and pro-apoptotic activities of SNG in a panel of MM cell lines (U266, IM9, MM1S, and RPMI-8226). SNG treatment of MM cells resulted in a dose-dependent decrease in cell viability through mitochondrial membrane potential loss and activation of caspase 3, 9, and cleavage of PARP. Pre-treatment of MM cells with a universal caspase inhibitor, Z-VAD-FMK, prevented SNG mediated loss of cell viability, apoptosis, and caspase activation, confirming that SNG-mediated apoptosis is caspase-dependent. The SNG-mediated apoptosis appears to be resulted from suppres...
Source: Frontiers in Oncology - April 16, 2019 Category: Cancer & Oncology Source Type: research

SMAD4 gene mutation renders pancreatic cancer resistance to radiotherapy through promotion of autophagy.
CONCLUSIONS: Our results demonstrate that defective SMAD4 is responsible for radioresistance in pancreatic cancer through induction of ROS and increased level of radiation-induced autophagy. PMID: 29602802 [PubMed - as supplied by publisher]
Source: Clinical Cancer Research - March 30, 2018 Category: Cancer & Oncology Authors: Wang F, Xia X, Yang C, Shen J, Mai J, Kim HC, Kirui D, Kang Y, Fleming JB, Koay EJ, Mitra S, Ferrari M, Shen H Tags: Clin Cancer Res Source Type: research

Silibinin sensitizes TRAIL-mediated apoptosis by upregulating DR5 through ROS-induced endoplasmic reticulum stress-Ca2+-CaMKII-Sp1 pathway.
In this study, we addressed how silibinin enhances tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-mediated apoptosis in various cancer cells. Combined treatment with silibinin and TRAIL (silibinin/TRAIL) induced apoptosis accompanied by the activation of caspase-3, caspase-8, caspase-9, and Bax, and cytosolic accumulation of cytochrome c. Anti-apoptotic proteins such as Bcl-2, IAP-1, and IAP-2 were inhibited as well. Silibinin also triggered TRAIL-induced apoptosis in A549 cells through upregulation of death receptor 5 (DR5). Pretreatment with DR5/Fc chimeric protein and DR5-targeted small interfering RNA ...
Source: Oncotarget - March 16, 2018 Category: Cancer & Oncology Tags: Oncotarget Source Type: research

TGF- β1-induced cell migration in pancreatic carcinoma cells is RAC1 and NOX4-dependent and requires RAC1 and NOX4-dependent activation of p38 MAPK.
TGF-β1-induced cell migration in pancreatic carcinoma cells is RAC1 and NOX4-dependent and requires RAC1 and NOX4-dependent activation of p38 MAPK. Oncol Rep. 2017 Oct 12;: Authors: Witte D, Bartscht T, Kaufmann R, Pries R, Settmacher U, Lehnert H, Ungefroren H Abstract Transforming growth factor (TGF)-β promotes epithelial-mesenchymal transition and cell invasion of cancer cells in part through the small GTPase RAC1. Since RAC1 can signal through reactive oxygen species (ROS), we probed the role of the ROS-producing NADPH oxidase (NOX) and p38 mitogen-activated protein kinase (MAPK) in mediating TG...
Source: Oncology Reports - October 20, 2017 Category: Cancer & Oncology Tags: Oncol Rep Source Type: research

Kaempferol induces ATM/p53-mediated death receptor and mitochondrial apoptosis in human umbilical vein endothelial cells.
In this study, we investigated the role of kaempferol on anti-angiogenic property and the apoptotic mechanism of human umbilical vein endothelial cells (HUVECs). Our results demonstrated that kaempferol decreased HUVEC viability in a time- and concentration-dependent manner. Kaempferol also induced morphological changes and sub-G1 phase cell population (apoptotic cells). Kaempferol triggered apoptosis of HUVECs as detecting by DNA fragmentation, comet assay and immunofluorescent staining for activated caspase-3. The caspase signals, including caspase-8, -9 and -3, were time-dependently activated in HUVECs after kaempferol ...
Source: International Journal of Oncology - March 4, 2016 Category: Cancer & Oncology Authors: Lee CF, Yang JS, Tsai FJ, Chiang NN, Lu CC, Huang YS, Chen C, Chen FA Tags: Int J Oncol Source Type: research

Evaluation of HO-1 expression, cellular ROS production, cellular proliferation and cellular apoptosis in human esophageal squamous cell carcinoma tumors and cell lines.
Authors: Ren QG, Yang SL, Hu JL, Li PD, Chen YS, Wang QS Abstract Patients with esophageal squamous cell carcinoma (ESCC) have a poor prognosis. However, the related mechanisms are unclear, thus we investigated the expression of HO-1 in ESCC tissue and explored possible mechanisms of tumor progression. Expression of HO-1 was examined by immunohistochemistry in 143 ESCC tumors. The correlation of HO-1 with clinicopathological characteristics was also examined. Two human ESCC cell lines, TE-13 and Eca109 were studied. Silencing of cell line HO-1 by specific small interfering RNA (siRNA) was evaluated using real-time...
Source: Oncology Reports - January 21, 2016 Category: Cancer & Oncology Tags: Oncol Rep Source Type: research

Reactive oxygen species production has a critical role in hypoxia-induced Stat3 activation and angiogenesis in human glioblastoma
In this study, we explored the possible implication of reactive oxygen species (ROS) in hypoxia-driven Stat3 activation in human glioblastoma. We found that hypoxic stress increased ROS production as well as Stat3 activation and that ROS inhibitors (diphenyleneiodonium, rotenone and myxothiazol) and an antioxidant (N-acetyl-l-cysteine) blocked Stat3 activation under hypoxic conditions. To determine a major route of ROS production, we tested whether nicotinamide adenine dinucleotide phosphate oxidase 4 (Nox4) is involved in hypoxia-induced ROS production. Nox4 expression was found to be increased at both mRNA and protein le...
Source: Journal of Neuro-Oncology - August 21, 2015 Category: Cancer & Oncology Source Type: research

Abstract 4379: MPT0B292 enhances acetylation of {alpha}-tubulin through up-regulation of acetyltransferase gene, MEC-17 and exhibits potent anti-tumor, anti-angiogenesis and anti-metastatic effects in vitro and in vivo
In recent years, epigenetic therapeutics is a new generation of chemotherapeutics for cancer. Microtubule-targeted agents constitute a type of anticancer drugs largely used in the clinics. Cells generate distinct microtubule subtypes through expression of different iso-types and through post-translational modifications, including acetylation, detyrosination, polyglutamination and polyglycylation. The acetylation of α-tubulin K-40 is controlled by the balance between acetyltransferase and de-acetylase expression. MEC-17, one of α-tubulin acetyltransferases, plays an important role in the regulation of acetylation of α-tu...
Source: Cancer Research - August 2, 2015 Category: Cancer & Oncology Authors: Chang, J.-Y., Cheng, Y.-C. Tags: Experimental and Molecular Therapeutics Source Type: research

Synergistic Effect of Sulindac and Simvastatin on Apoptosis in Lung Cancer A549 Cells through ...
Conclusion Combined treatment with sulindac and simvastatin augmented their apoptotic potential in lung cancer cells through AKT signaling-dependent downregulation of survivin. These results indicate that sulindac and simvastatin may be clinically promising therapies for the prevention of lung cancer.
Source: Cancer Research and Treatment - October 26, 2014 Category: Cancer & Oncology Tags: Original Article Source Type: research

Abstract 493: NRF2 modulates sensitivity to thymidylate synthase inhibitors in colon cancer cells
Thymidylate synthase (TYMS) catalyzes the reductive methylation of dUMP, and is the sole de novo source of thymidine for DNA replication and repair. As such, it is an important target of chemotherapeutic drugs, particularly the fluoropyrimidines 5-fluorouracil (FUra) and 5-fluoro-2’-deoxyuridine (FdUrd), as well as the folate analog raltitrexed (RTX). In cells, these drugs are metabolized to derivatives that bind to and inhibit TYMS, leading to depletion of thymidine levels, dysregulation of redox metabolism, generation of oxidative stress, and, eventually, apoptotic cell death. Gene expression profiles of FUra-treated H...
Source: Cancer Research - September 30, 2014 Category: Cancer & Oncology Authors: Clinton, S. A., Barbour, K. W., Ozer, U., Berger, F. G. Tags: Molecular and Cellular Biology Source Type: research

Effect of hypoxia on the expression of alphaB-crystallin in head and neck squamous cell carcinoma
Conclusions: We provide the first evidence that hypoxia stimulates upregulation of alphaB-crystallin in HNSCC. This upregulation was not caused by the low oxygen pressure, but more likely by ROS formation. The higher expression of alphaB-crystallin may lead to prolonged survival of these cells under hypoxic conditions.
Source: BMC Cancer - April 11, 2014 Category: Cancer & Oncology Authors: Chantal van de SchootbruggeElisabeth SchultsJohan BussinkPaul SpanReidar GrénmanGer PruijnJohannes KaandersWilbert Boelens Source Type: research