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Arsenic trioxide disturbs the LIS1/NDEL1/dynein microtubule dynamic complex by disrupting the CLIP170 zinc finger in head and neck cancer.
Abstract Cancer mortality is mainly caused by metastasis, which requires dynamic remodeling of cytoskeletal components such as microtubules. Targeting microtubules presents a promising antimetastatic strategy that could prevent cancer spreading and recurrence. It is known that arsenic trioxide (ATO) is able to inhibit the migration and invasion of solid malignant tumors, but its exact molecular mechanism remains unclear. Here, we report a novel molecular target and antimetastatic mechanism of ATO in head and neck squamous cell carcinoma (HNSCC). We found that cytoplasmic linker protein 170 (CLIP170) was overexpres...
Source: Toxicology and Applied Pharmacology - July 23, 2020 Category: Toxicology Authors: Gao L, Xue B, Xiang B, Liu KJ Tags: Toxicol Appl Pharmacol Source Type: research

ROS -mediated p53 activation by juglone enhances apoptosis and autophagy in vivo and in vitro.
Abstract Juglone (JG) exhibits a broad-spectrum of cytotoxicity against some cancer cells. However, its molecular mechanisms have not been investigated well. Here, the present results showed that JG significantly inhibited tumor growth in vivo. CCK-8 assays, flow cytometric analysis, western blotting and immunohistochemistry revealed that JG effectively inhibited cell proliferation and induced apoptosis through extrinsic pathways. We also observed that JG treatment induced autophagy flux via activiting the AMPK-mTOR signaling pathway. In addition, we found that JG enhanced p53 activation by increasing down-regulat...
Source: Toxicology and Applied Pharmacology - July 4, 2019 Category: Toxicology Authors: Wang P, Zhang SD, Jiao J, Wang W, Yu L, Zhao XL, Wang LT, Meng D, Fu YJ Tags: Toxicol Appl Pharmacol Source Type: research

Role of Mcl-1 in regulation of cell death in human induced pluripotent stem cell-derived cardiomyocytes in vitro.
Abstract Targeting the anti-apoptotic protein Mcl-1 holds a promise to improve therapy of multiple types of Mcl-1 dependent cancers but raises concerns of on-target cardiotoxicity due to the presence and reported role of Mcl-1 in heart. Herein, we investigated the importance of Mcl-1 in the survival and contractile function of human pluripotent stem cell-derived cardiomyocytes in culture. Effective knockdown of Mcl-1 with siRNAs reproducibly resulted in early (measured at Day 3) marginal alterations in caspase 3/7 activity, LDH leakage, ATP content and cellular impedance. After 14 days of Mcl-1 knockdown, loss o...
Source: Toxicology and Applied Pharmacology - September 27, 2018 Category: Toxicology Authors: Guo L, Eldridge S, Furniss M, Mussio J, Davis M Tags: Toxicol Appl Pharmacol Source Type: research

Raddeanin A, a natural triterpenoid saponin compound, exerts anticancer effect on human osteosarcoma via the ROS/JNK and NF- κB signal pathway.
Raddeanin A, a natural triterpenoid saponin compound, exerts anticancer effect on human osteosarcoma via the ROS/JNK and NF-κB signal pathway. Toxicol Appl Pharmacol. 2018 May 27;: Authors: Ma B, Zhu J, Zhao A, Zhang J, Wang Y, Zhang H, Zhang L, Zhang Q Abstract Osteosarcoma (OS) is the most frequent and high mortality primary bone tumor in the adolescent. And it is well-known for poor prognosis due to high incidence of metastasis. Raddeanin A (RA), an active component of Anemone raddeana Regel, showed potential anti-cancer activities. However, the anti-tumor effect and molecular mechanism(s) of RA o...
Source: Toxicology and Applied Pharmacology - May 27, 2018 Category: Toxicology Authors: Ma B, Zhu J, Zhao A, Zhang J, Wang Y, Zhang H, Zhang L, Zhang Q Tags: Toxicol Appl Pharmacol Source Type: research

Impaired autophagic flux and p62-mediated EMT are involved in arsenite-induced transformation of L-02 cells.
Abstract Autophagy is a catabolic process essential for preserving cellular homeostasis, and the epithelial-to-mesenchymal transition (EMT) is involved during tissue development and cancer progression. In arsenite-treated human hepatic epithelial (L-02) cells, arsenite reduced the autophagic flux, which caused accumulation of p62, an adaptor and receptor of autophagy. Further, in arsenite-transformed L-02 cells, the levels of E-cadherin were attenuated, but the levels of vimentin, which is expressed in mesenchymal cells, and Snail, a transcription regulator of the EMT, were up-regulated. Thus, after chronic exposu...
Source: Toxicology and Applied Pharmacology - September 6, 2017 Category: Toxicology Authors: Liu X, Ling M, Chen C, Luo F, Yang P, Wang D, Chen X, Xu H, Xue J, Yang Q, Lu L, Lu J, Bian Q, Zhang A, Liu Q Tags: Toxicol Appl Pharmacol Source Type: research

Methylation of Septin9 Mediated by DNMT3a Enhances Hepatic Stellate Cells Activation and Liver Fibrogenesis.
Abstract Liver fibrosis, resulting from chronic and persistent injury to the liver, is a worldwide health problem. Advanced liver fibrosis results in cirrhosis, liver failure and even hepatocellular cancer (HCC), often eventually requiring liver transplantation, poses a huge health burden on the global community. However, the specific pathogenesis of liver fibrosis remains not fully understood. Numerous basic and clinical studies have provided evidence that epigenetic modifications, especially DNA methylation, might contribute to the activation of hepatic stellate cells (HSCs), the pivotal cell type responsible fo...
Source: Toxicology and Applied Pharmacology - December 5, 2016 Category: Toxicology Authors: Wu Y, Bu F, Yu H, Li W, Huang C, Meng X, Zhang L, Ma T, Li J Tags: Toxicol Appl Pharmacol Source Type: research

Characterization of acquired paclitaxel resistance of breast cancer cells and involvement of ABC transporters.
Abstract Development of taxane resistance has become clinically very important issue. The molecular mechanisms underlying the resistance are still unclear. To address this issue, we established paclitaxel-resistant sublines of the SK-BR-3 and MCF-7 breast cancer cell lines that are capable of long-term proliferation in 100nM and 300nM paclitaxel, respectively. Application of these concentrations leads to cell death in the original counterpart cells. Both sublines are cross-resistant to doxorubicin, indicating the presence of the MDR phenotype. Interestingly, resistance in both paclitaxel-resistant sublines is circ...
Source: Toxicology and Applied Pharmacology - September 20, 2016 Category: Toxicology Authors: Němcová-Fürstová V, Kopperová D, Balušíková K, Ehrlichová M, Brynychová V, Václavíková R, Daniel P, Souček P, Kovář J Tags: Toxicol Appl Pharmacol Source Type: research

Arsenic silences hepatic PDK4 expression through activation of histone H3K9 methylatransferase G9a.
Abstract It is well established that increased liver cancer incidence is strongly associated with epigenetic silencing of tumor suppressor genes; the latter is contributed by the environmental exposure to arsenic. Pyruvate dehydrogenase kinase 4 (PDK4) is a mitochondrial protein that regulates the TCA cycle. However, the epigenetic mechanisms mediated by arsenic to control PDK4 expression remain elusive. In the present study, we showed that histone methyltrasferase G9a- and Suv39H-mediated histone H3 lysine 9 (H3K9) methylations contributed to PDK4 silencing in hepatic cells. The PDK4 expression was induced by G9a...
Source: Toxicology and Applied Pharmacology - May 19, 2016 Category: Toxicology Authors: Zhang X, Wu J, Choiniere J, Yang Z, Huang Y, Bennett J, Wang L Tags: Toxicol Appl Pharmacol Source Type: research

Epigenetic silencing of miR-218 by the lncRNA CCAT1, acting via BMI1, promotes an altered cell cycle transition in the malignant transformation of HBE cells induced by cigarette smoke extract.
Abstract Cigarette smoking is the strongest risk factor for the development of lung cancer, the leading cause of cancer-related deaths. However, the molecular mechanisms leading to lung cancer are largely unknown. A long-noncoding RNA (lncRNA), CCAT1, regarded as cancer-associated, has been investigated extensively. Moreover, the molecular mechanisms of lncRNAs in regulation of microRNAs (miRNAs) induced by cigarette smoke remain unclear. In the present investigation, cigarette smoke extract (CSE) caused an altered cell cycle and increased CCAT1 levels and decreased miR-218 levels in human bronchial epithelial (HB...
Source: Toxicology and Applied Pharmacology - May 18, 2016 Category: Toxicology Authors: Lu L, Xu H, Luo F, Liu X, Lu X, Yang Q, Xue J, Chen C, Shi L, Liu Q Tags: Toxicol Appl Pharmacol Source Type: research

Continuous activation of Nrf2 and its target antioxidant enzymes leads to arsenite-induced malignant transformation of human bronchial epithelial cells.
Abstract Long-term exposure to arsenite leads to human lung cancer, but the underlying mechanisms of carcinogenesis remain obscure. The transcription factor of nuclear factor-erythroid-2 p45-related factor (Nrf2)-mediated antioxidant response represents a critical cellular defense mechanism and protection against various diseases. Paradoxically, emerging data suggest that the constitutive activation of Nrf2 is associated with cancer development, progression and chemotherapy resistance. However, the role of Nrf2 in the occurrence of cancer induced by long-term arsenite exposure remains to be fully understood. By es...
Source: Toxicology and Applied Pharmacology - September 26, 2015 Category: Toxicology Authors: Yang X, Wang D, Ma Y, Xu X, Zhu Z, Wang X, Deng H, Li C, Chen M, Tong J, Yamanaka K, An Y Tags: Toxicol Appl Pharmacol Source Type: research

Posttranscriptional silencing of the lncRNA MALAT1 by miR-217 inhibits the epithelial-mesenchymal transition via enhancer of zeste homolog 2 in the malignant transformation of HBE cells induced by cigarette smoke extract.
Abstract Lung cancer is regarded as the leading cause of cancer-related deaths, and cigarette smoking is one of the strongest risk factors for the development of lung cancer. However, the mechanisms for cigarette smoke-induced lung carcinogenesis remain unclear. The present study investigated the effects of an miRNA (miR-217) on levels of an lncRNA (MALAT1) and examined the role of these factors in the epithelial-mesenchymal transition (EMT) induced by cigarette smoke extract (CSE) in human bronchial epithelial (HBE) cells. In these cells, CSE caused decreases of miR-217 levels and increases in lncRNA MALAT1 level...
Source: Toxicology and Applied Pharmacology - September 25, 2015 Category: Toxicology Authors: Lu L, Luo F, Liu Y, Liu X, Shi L, Lu X, Liu Q Tags: Toxicol Appl Pharmacol Source Type: research

Cadmium promotes the proliferation of triple-negative breast cancer cells through EGFR-mediated cell cycle regulation.
Abstract Cadmium (Cd) is a carcinogenic metal which is implicated in breast cancer by epidemiological studies. It is reported to promote breast cancer cell growth in vitro through membrane receptors. The study described here examined Cd-mediated growth of non-metastatic human breast cancer derived cells that lack receptors for estrogen, progesterone, and HER2. Treatment of triple-negative HCC 1937 cells with 0.1-0.5μM Cd increased cell growth by activation of AKT and ERK. Accelerated cell cycle progression was achieved by increasing the levels of cyclins A, B, and E, as well as those of CDKs 1 and 2. Although tri...
Source: Toxicology and Applied Pharmacology - September 15, 2015 Category: Toxicology Authors: Wei Z, Song X, Shaikh ZA Tags: Toxicol Appl Pharmacol Source Type: research

Requirement of ERα and Basal Activities of EGFR and Src Kinase in Cd-induced Activation of MAP/ERK Pathway in Human Breast Cancer MCF-7 Cells.
This study explores the mechanism of Cd-induced activation of MAPK/ERK pathway. Specifically, the role of cell surface receptors ERα, EGFR, and Src kinase was evaluated in human breast cancer MCF-7 cells treated with 1-3 μM Cd. The activation of ERK was studied using a serum response element (SRE) luciferase reporter assay. Receptor phosphorylation was detected by Western blot analyses. Cd treatment increased both the SRE reporter activity and ERK1/2 phosphorylation in a concentration-dependent manner. Cd treatment had no effect on reactive oxygen species (ROS) generation. Also, blocking the entry of Cd into the cells wi...
Source: Toxicology and Applied Pharmacology - May 22, 2015 Category: Toxicology Authors: Song X, Wei Z, Shaikh ZA Tags: Toxicol Appl Pharmacol Source Type: research

Combined effects of EGFR tyrosine kinase inhibitors and vATPase inhibitors in NSCLC cells.
Abstract Despite excellent initial clinical responses of non-small cell lung cancer (NSCLC) patients to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs), many patients eventually develop resistance. According to a recent report, vacuolar H+ ATPase (vATPase) is overexpressed and is associated with chemotherapy drug resistance in NSCLC. We investigated the combined effects of EGFR TKIs and vATPase inhibitors and their underlying mechanisms in the regulation of NSCLC cell death. We found that combined treatment with EGFR TKIs (erlotinib, gefitinib, or lapatinib) and vATPase inhibitors (bafilo...
Source: Toxicology and Applied Pharmacology - May 14, 2015 Category: Toxicology Authors: Jin HO, Hong SE, Kim CS, Park JA, Kim JH, Kim JY, Kim B, Chang YH, Hong SI, Hong YJ, Park IC, Lee JK Tags: Toxicol Appl Pharmacol Source Type: research

Dopamine induces growth inhibition and vascular normalization through reprograming M2-polarized macrophages in rat C6 glioma.
Abstract Dopamine (DA), a monoamine catecholamine neurotransmitter with antiangiogenic activity, stabilizes tumor vessels in colon, prostate and ovarian cancer, thus increases chemotherapeutic efficacy. Here, in the rat C6 glioma models, we investigated the vascular normalization effects of DA and its mechanisms of action. DA (25, 50 mg/kg) inhibited tumor growth, while a precursor of DA (levodopa) prolonged the survival time of rats bearing orthotopic C6 glioma. DA improved tumor perfusion, with significant effects from day 3, and a higher level at day 5 to 7. In addition, DA decreased microvessel density and hyp...
Source: Toxicology and Applied Pharmacology - March 25, 2015 Category: Toxicology Authors: Qin T, Wang C, Chen X, Duan C, Zhang X, Zhang J, Chai H, Tang T, Chen H, Yue J, Li Y, Yang J Tags: Toxicol Appl Pharmacol Source Type: research

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