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Specialty: Toxicology
Cancer: Lung Cancer

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Total 20 results found since Jan 2013.

Gossypol enhances the efficacy of sorafenib by trigging autophagy and apoptosis in metastatic lung cancer cells: An upshot of Chou-Talalay combination index process
In conclusion combination of gossypol and sorafenib shows synergistic increase in the cytotoxic effect by promoting autophagy and apoptosis.PMID:37611852 | DOI:10.1016/j.tiv.2023.105666
Source: Toxicology in Vitro - August 23, 2023 Category: Toxicology Authors: Yusuf Hussain Abha Meena Rohit Anthony Sinha Source Type: research

Involvement of m6A regulatory factor IGF2BP1 in malignant transformation of human bronchial epithelial Beas-2B cells induced by tobacco carcinogen NNK
This study therefore contributes novel insights into the environmental pathogenesis of lung cancer and the gene regulatory mechanisms of chemical carcinogenesis.PMID:34974052 | DOI:10.1016/j.taap.2021.115849
Source: Toxicology and Applied Pharmacology - January 2, 2022 Category: Toxicology Authors: Jiaxin Zhou Rui Xiong Jiazhen Zhou Xinchao Guan Guanqing Jiang Yuyang Chen Qiaoyuan Yang Source Type: research

Involvement of twist in NNK exposure-promoted lung cancer cell migration and invasion.
In conclusion, Twist was involved in NNK-induced migration and invasion of lung cancer cells. PMID: 31759049 [PubMed - as supplied by publisher]
Source: Toxicology in Vitro - November 19, 2019 Category: Toxicology Authors: Wang Y, Shi L, Li J, Wang H, Yang H Tags: Toxicol In Vitro Source Type: research

Inhibition of thymidine phosphorylase expression by Hsp90 inhibitor potentiates the cytotoxic effect of salinomycin in human non-small-cell lung cancer cells.
In this study, we report whether Hsp90 inhibitor 17-AAG could enhance salinomycin-induced cytotoxicity in NSCLC cells through modulating TP expression in two non-small-cell lung cancer (NSCLC) cell lines, A549 and H1975. We found that salinomycin increased TP expression in a MKK3/6-p38 MAPK activation manner. Knockdown of TP using siRNA or inactivation of p38 MAPK by pharmacological inhibitor SB203580 enhanced the cytotoxic and growth inhibition effects of salinomycin. In contrast, enforced expression of MKK6E (a constitutively active form of MKK6) reduced the cytotoxicity and cell growth inhibition of salinomycin. Moreove...
Source: Toxicology - February 20, 2019 Category: Toxicology Authors: Ko JC, Chen JC, Chen TY, Yen TC, Ma PF, Lin YC, Wu CH, Peng YS, Zheng HY, Lin YW Tags: Toxicology Source Type: research

Perfluoroalkyl acid exposure induces protective mitochondrial and endoplasmic reticulum autophagy in lung cells.
In this study, lung cancer cells, A549, were employed as the model to investigate the effects of three PFAAs with different carbon chain lengths on cell autophagy. Through Western blot analysis on LC3-I/II ratio of cells exposed to non-cytotoxic concentration (200 µM) and cytotoxic concentration (350 µM), we found concentration-dependent increase of autophagosomes in cells, which was further confirmed by TEM examination on ultra-thin section of cells and fluorescence imaging on autophagosomes in live cells. The abundance of p62 increased with the PFAAs concentration indicating the blockage of autophagy flux. Furthermor...
Source: Archives of Toxicology - July 18, 2018 Category: Toxicology Authors: Xin Y, Wan B, Yang Y, Cui XJ, Xie YC, Guo LH Tags: Arch Toxicol Source Type: research

The role of SerpinB2 in human bronchial epithelial cells responses to particulate matter exposure.
In conclusion, here we show that PAI-2 regulates CDH1 gene/cadherin-1 protein expression in bronchial HBEC3-KT cells, and this mechanism might be involved in the regulation of cell migration. SERPINB2 down-regulation should be considered part of EMT, and the over-expression of SERPINB2 in PM-exposed samples might be interpreted as an initial protective mechanism. PMID: 29987410 [PubMed - as supplied by publisher]
Source: Archives of Toxicology - July 9, 2018 Category: Toxicology Authors: Longhin E, Camatini M, Bersaas A, Mantecca P, Mollerup S Tags: Arch Toxicol Source Type: research

Involvement of HIF-1 α-regulated miR-21, acting via the Akt/NF-κB pathway, in malignant transformation of HBE cells induced by cigarette smoke extract.
Involvement of HIF-1α-regulated miR-21, acting via the Akt/NF-κB pathway, in malignant transformation of HBE cells induced by cigarette smoke extract. Toxicol Lett. 2018 Feb 28;: Authors: Lu L, Xu H, Yang P, Xue J, Chen C, Sun Q, Yang Q, Lu J, Shi A, Liu Q Abstract Although the relationship between cigarette smoke and lung cancer has been widely studied, the molecular mechanism for cigarette smoke-induced lung cancer remains largely unclear. The present study investigated the roles of hypoxia-inducible factor (HIF)-1α and miR-21 in the malignant transformation of human bronchial epithelial (HBE) ce...
Source: Toxicology Letters - February 28, 2018 Category: Toxicology Authors: Lu L, Xu H, Yang P, Xue J, Chen C, Sun Q, Yang Q, Lu J, Shi A, Liu Q Tags: Toxicol Lett Source Type: research

Astaxanthin enhances pemetrexed-induced cytotoxicity by downregulation of thymidylate synthase expression in human lung cancer cells
In this study, we showed that down-regulating of TS expression in two NSCLC cell lines, human lung adenocarcinoma H1650 and squamous cell carcinoma H1703 cells, with astaxanthin were associated with decreased MKK1/2-ERK1/2 activity. Enforced expression of constitutively active MKK1 (MKK1-CA) vector significantly rescued the decreased TS mRNA and protein levels in astaxanthin-treated NSCLC cells. Combined treatment with a MKK1/2 inhibitor (U0126 or PD98059) further decreased the TS expression in astaxanthin-exposed NSCLC cells. Knockdown of TS using small interfering RNA (siRNA) or inhibiting ERK1/2 activity enhanced the c...
Source: Regulatory Toxicology and Pharmacology - October 1, 2016 Category: Toxicology 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

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

Alpha5 nicotinic acetylcholine receptor mediates nicotine-induced HIF-1α and VEGF expression in non-small cell lung cancer.
Abstract By binding to nicotinic acetylcholine receptors (nAChRs), nicotine induces the proliferation and apoptosis of non-small cell lung cancer (NSCLC). Previous studies have indicated that α5-nAChR is highly associated with lung cancer risk and nicotine dependence. However, the mechanisms through which α5-nAChRs may influence lung carcinogenesis are far from clear. In the present study, we investigated the roles of α5-nAChR in the nicotine-induced expression of hypoxia-inducible factor-1α (HIF-1α) and vascular endothelial growth factor (VEGF). Immunohistochemistry was used to detect the expression of α5-n...
Source: Toxicology and Applied Pharmacology - April 30, 2014 Category: Toxicology Authors: Ma X, Jia Y, Zu S, Li R, Jia Y, Zhao Y, Xiao D, Dang N, Wang Y Tags: Toxicol Appl Pharmacol Source Type: research