αvβ3 Integrin-Mediated Drug Resistance in Human Laryngeal Carcinoma Cells Is Caused by Glutathione-Dependent Elimination of Drug-Induced Reactive Oxidative Species

2008 ◽  
Vol 74 (1) ◽  
pp. 298-306 ◽  
Author(s):  
Anamaria Brozović ◽  
Dragomira Majhen ◽  
Vibor Roje ◽  
Nevenka Mikac ◽  
Sanjica Jakopec ◽  
...  
Keyword(s):  
Drug Resistance ◽  
Laryngeal Carcinoma ◽  
Carcinoma Cells ◽  
Αvβ3 Integrin ◽  
Reactive Oxidative Species ◽  
Drug Induced ◽  
Human Laryngeal Carcinoma ◽  
Oxidative Species

scholarly journals Genotoxic Effects of Green Tea Extract on Human Laryngeal Carcinoma Cells In Vitro

2011 ◽  
Vol 62 (2) ◽  
pp. 139-146 ◽  
Author(s):  
Ksenija Durgo ◽  
Sandra Kostić ◽  
Katarina Gradiški ◽  
Draženka Komes ◽  
Maja Osmak ◽  
...  
Keyword(s):  
Cell Line ◽  
Green Tea ◽  
Laryngeal Carcinoma ◽  
Resistant Cell ◽  
Resistant Cell Line ◽  
Green Tea Extract ◽  
Carcinoma Cells ◽  
Tea Extract ◽  
Human Laryngeal Carcinoma

Genotoxic Effects of Green Tea Extract on Human Laryngeal Carcinoma Cells In VitroGreen tea (Camellia sinensis) contains several bioactive compounds which protect the cell and prevent tumour development. Phytochemicals in green tea extract (mostly flavonoids) scavenge free radicals, but also induce pro-oxidative reactions in the cell. In this study, we evaluated the potential cytotoxic and prooxidative effects of green tea extract and its two main flavonoid constituents epigallocatechin gallate (EGCG) and epicatechin gallate (ECG) on human laryngeal carcinoma cell line (HEp2) and its cross-resistant cell line CK2. The aim was to see if the extract and its two flavonoids could increase the sensitivity of the cisplatin-resistant cell line CK2 in comparison to the parental cell line. The results show that EGCG and green tea extract increased the DNA damage in the CK2 cell line during short exposure. The cytotoxicity of EGCG and ECG increased with the time of incubation. Green tea extract induced lipid peroxidation in the CK2 cell line. The pro-oxidant effect of green tea was determined at concentrations higher than those found in traditionally prepared green tea infusions.

Oxidative Stress in HEp-2 Human Laryngeal Carcinoma Cells Induced by Combination of Vitamins B12b and C

2003 ◽  
Vol 136 (3) ◽  
pp. 279-282 ◽  
Author(s):  
V. S. Akatov ◽  
M. E. Solov'eva ◽  
V. V. Leshchenko ◽  
V. V. Teplova
Keyword(s):  
Oxidative Stress ◽  
Laryngeal Carcinoma ◽  
Carcinoma Cells ◽  
Human Laryngeal Carcinoma

Suppression of Survivin Expression by Short Hairpin RNA Induces Apoptosis in Human Laryngeal Carcinoma Cells

ORL ◽  
2008 ◽  
Vol 70 (3) ◽  
pp. 168-175 ◽  
Author(s):  
Xiu-mei Chen ◽  
Xin-yong Luan ◽  
Da-peng Lei ◽  
Xiao-jie Ma ◽  
Xue-xia Liu ◽  
...  
Keyword(s):  
Laryngeal Carcinoma ◽  
Survivin Expression ◽  
Short Hairpin Rna ◽  
Carcinoma Cells ◽  
Hairpin Rna ◽  
Short Hairpin ◽  
Human Laryngeal Carcinoma

scholarly journals Effect and Mechanism of Survivin on Hypoxia-Induced Multidrug Resistance of Human Laryngeal Carcinoma Cells

2019 ◽  
Vol 2019 ◽  
pp. 1-6
Author(s):  
Dan Xu ◽  
Da Wei Li ◽  
Jin Xie ◽  
Xin Wei Chen
Keyword(s):  
Multidrug Resistance ◽  
Rna Interference ◽  
Cancer Cells ◽  
Propidium Iodide ◽  
Laryngeal Carcinoma ◽  
Survivin Expression ◽  
Annexin V ◽  
Carcinoma Cells ◽  
Propidium Iodide Staining ◽  
Human Laryngeal Carcinoma

This study aimed at clarifying the mechanism and role of survivin in hypoxia-induced multidrug resistance (MDR) of laryngeal carcinoma cells. Human laryngeal cancer cells were incubated under hypoxia or normoxia. The expression of survivin was silenced by performing RNA interference. Additionally, by Western blot and real-time quantitative RT-PCR, survivin expression was detected. The sensitivity of human laryngeal carcinoma cells to multiple drugs was measured by CCK-8 assay. Meanwhile, the apoptosis of cells induced by cisplatin or paclitaxel was assessed by Annexin-V/propidium iodide staining analysis. Under hypoxic conditions, the upregulation of survivin was abolished by RNA interference. Then, CCK-8 analysis demonstrated that the sensitivity to multiple agents of laryngeal carcinoma cells could be increased by inhibiting survivin expression (P<0.05). Moreover, Annexin-V/propidium iodide staining analysis revealed that decreased expression of survivin could evidently increase the apoptosis rate of laryngeal carcinoma cells that were induced by cisplatin or paclitaxel evidently (P<0.05). Our data suggests that hypoxia-elicited survivin may exert a pivotal role in regulating hypoxia-induced MDR of laryngeal cancer cells by preventing the apoptosis of cells induced by chemotherapeutic drug. Thus, blocking survivin expression in human laryngeal carcinoma cells may provide an avenue for gene therapy.

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