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.

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 Notch1 Signaling Modulates Hypoxia-induced Multidrug Resistance of Human Laryngeal Cancer Cells

2021 ◽  
Author(s):  
Dawei Li ◽  
Dan Xu ◽  
Penghui Chen ◽  
Jin Xie
Keyword(s):  
Multidrug Resistance ◽  
Cancer Cells ◽  
Laryngeal Cancer ◽  
Laryngeal Carcinoma ◽  
Drug Transport ◽  
Malignant Tumors ◽  
Carcinoma Cells ◽  
Cell Counting ◽  
Apoptosis Resistance ◽  
Notch1 Signaling

Abstract Background: Laryngeal carcinoma is one of the common malignant tumors of the head and neck. Multidrug resistance (MDR) remains a critical problem in the chemotherapy for patients with laryngeal cancer. This study aims to clarify the role and mechanisms of Notch1 signaling on MDR induced by hypoxia in laryngeal cancer cells.Methods and Results: Laryngeal carcinoma cells were cultured under normoxia or hypoxia. Notch1 expression was inhibited by small interfering RNA (siRNA). The expression of Notch1, Hes1, Hey1, MDR1 and survivin mRNA was determined by Real-time PCR. The expression of Notch1, Notch1 intracellular domain (N1ICD), MDR1/P-gp and survivin protein was detected by Western blot. Current research showed that hypoxia could upregulate Notch1 expression and the activity of Notch1 signaling. Furthermore, suppression of Notch1 expression could effectively down-regulate the activity of Notch1 signaling and the expression of MDR and survivin genes in laryngeal cancer cells under hypoxia (P<0.05). Cell Counting Kit-8 (CCK-8) assay confirmed that the sensitivity of hypoxic laryngeal cancer cells to a variety of drugs could be up-regulated by suppressing Notch1 expression (P<0.05). Additionally, flow cytometry (FCM) showed that suppression of Notch1 expression significantly increased cisplatin-induced apoptosis and intracellular Rh123 (Rh123) accumulation in hypoxic laryngeal carcinoma cells (P<0.05). Conclusions: Notch1 signalling could be regarded as a pivotal regulator for mediating hypoxia-induced MDR in laryngeal cancer cells by regulating survivin-mediated apoptosis resistance and MDR1/P-gp-mediated drug transport.

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.

scholarly journals Sodium citrate inhibits proliferation and induces apoptosis of hepatocellular carcinoma cells

2020 ◽  
Vol 7 (3) ◽  
pp. 3659-3666
Author(s):  
Phuc Hong Vo ◽  
Sinh Truong Nguyen ◽  
Nghia Minh Do ◽  
Kiet Dinh Truong ◽  
Phuc Van Pham
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cancer Cells ◽  
Dna Fragmentation ◽  
Hepg2 Cells ◽  
Annexin V ◽  
Carcinoma Cells ◽  
Human Gastric Cancer ◽  
Apoptosis Pathway ◽  
Hepatocellular Carcinoma Cells ◽  
Activation Assay

Introduction: Cancer cells rely on glycolysis to generate energy and synthesize biomass for cell growth and proliferation (the Warburg effect). Recent studies have shown that citrate has an inhibitory effect on several cancer cells, such as human gastric cancer and ovarian cancer, by inhibiting glycolysis. In this study, we investigated the effects of citrate on the proliferation and apoptosis induction of hepatocellular carcinoma cells. Methods: HepG2 hepatocellular carcinoma cell line was used in this study. The cell proliferation was evaluated by Alamar blue assay. The apoptotic status of the HepG2 cells was recorded by Annexin V/7-AAD assay and caspase 3/7 activation assay. DNA fragmentation was evaluated by nucleus staining assay with Hoechst 33342. Results: The results showed that citrate is able to inhibit the proliferation of HepG2 cells and induce apoptosis in these cells. The initiation time of apoptosis is 4 hours after treatment with 10 mM citrate. Morphology characteristics of DNA fragmentation and broken membranes were also recorded in the apoptotic cells. Conclusion: In conclusion, our study demonstrates that citrate causes HepG2 cell death by the apoptosis pathway.

scholarly journals Decrease in Multidrug Resistance-associated Protein 2 Activities by Knockdown of Phosphatidylinositol 4-phosphate 5-kinase in Hepatocytes and Cancer Cells

2019 ◽  
Vol 22 ◽  
pp. 576-584 ◽  
Author(s):  
Atsushi Kawase ◽  
Yuta Inoue ◽  
Miho Hirosoko ◽  
Yuka Sugihara ◽  
Hiroaki Shimada ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Multidrug Resistance ◽  
Cancer Cells ◽  
Hepg2 Cells ◽  
Carcinoma Cells ◽  
Efflux Transporters ◽  
Membrane Localization ◽  
Intracellular Accumulation ◽  
Primary Hepatocytes ◽  
Phosphatidylinositol 4

Purpose: The plasma membrane localization and transport activity of multidrug resistance-associated protein 2 (MRP2/ABCC2) and P-glycoprotein (P-gp/ABCB1) efflux transporters are governed by transporter-associated proteins. Phosphatidylinositol 4,5-bisphosphate (PIP2) formed by phosphatidylinositol 4-phosphate 5-kinase type 1 (PIP5K1) activates the linker function of radixin for efflux transporters. Radixin is involved in the plasma membrane localization of efflux transporters. We examined whether PIP5K1 could be a target for the modulation of transporter activities in hepatocytes and cancer cells. Methods: The effects of PIP5K1 depletion by siRNA in mouse primary hepatocytes, PANC1 human pancreatic carcinoma cells, and HepG2 human hepatocellular carcinoma cells on the intracellular accumulation of MRP2 and P-gp substrates were examined. Results: PIP5K1A depletion resulted in increased intracellular accumulation of carboxydichlorofluorescein, a MRP2 fluorescent substrate, in mouse primary hepatocytes, PANC1 cells, and HepG2 cells. In PANC1 and HepG2 cells, the transport activities of MRP2 were significantly decreased by PIP5K1C depletion. However, the transport activities of P-gp were unchanged by PIP5K1 depletion. PIP2 levels were unchanged between control and PIP5K1A- or PIP5K1C-depleted HepG2 cells. MRP2 mRNA levels showed few changes in HepG2 cells following PIP5K1A or PIP5K1C depletion. The expression of phosphorylated radixin was decreased by PIP5K1A and PIP5K1C depletion, although total radixin levels were unchanged. Conclusions: These data suggest that PIP5K1A and PIP5K1C could be target proteins for modulating MRP2 function, partly because of the resulting changes of the linker function of radixin.

Complete Reversal of ABCG2-Depending Atypical Multidrug Resistance by RNA Interference in Human Carcinoma Cells

2006 ◽  
Vol 16 (3) ◽  
pp. 263-274 ◽  
Author(s):  
Axel Priebsch ◽  
Franziska Rompe ◽  
Holger Tönnies ◽  
Petra Kowalski ◽  
Pawel Surowiak ◽  
...  
Keyword(s):  
Multidrug Resistance ◽  
Rna Interference ◽  
Carcinoma Cells ◽  
Human Carcinoma ◽  
Complete Reversal

scholarly journals Effects and mechanism of downregulation of survivin expression by RNA interference on proliferation and apoptosis of lung cancer cells

2012 ◽  
Vol 5 (4) ◽  
pp. 917-922 ◽  
Author(s):  
XIANG-QI CHEN ◽  
SHENG YANG ◽  
ZHI-YING LI ◽  
HUI-SHAN LU ◽  
MING-QIANG KANG ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Rna Interference ◽  
Cancer Cells ◽  
Survivin Expression ◽  
Lung Cancer Cells ◽  
Proliferation And Apoptosis

Annexin V staining during reperfusion detects cardiomyocytes with unique properties

2001 ◽  
Vol 281 (5) ◽  
pp. H1931-H1937 ◽  
Author(s):  
Prakash Narayan ◽  
Robert M. Mentzer ◽  
Robert D. Lasley
Keyword(s):  
Propidium Iodide ◽  
Ventricular Myocytes ◽  
Contractile Function ◽  
Ischemia Reperfusion ◽  
Annexin V ◽  
Cell Width ◽  
Simulated Ischemia ◽  
Propidium Iodide Staining ◽  
Membrane Blebs ◽  
Apoptosis And Necrosis

With the use of markers of sarcolemmal membrane permeability, cardiomyocyte models of ischemic injury have primarily addressed necrotic death during ischemia. In the present study, we used annexin V-propidium iodide staining to examine apoptosis and necrosis after simulated ischemia and simulated reperfusion in rat ventricular myocytes. Annexin V binds phosphatidylserine, a phosphoaminolipid thought to be externalized during apoptosis or programmed cell death. Propidium iodide is a marker of cell necrosis. Under baseline conditions, <1% of cardiomyocytes stained positive for annexin V. After 20 or 60 min of simulated ischemia, there was no increase in annexin V staining, although 60-min simulated ischemia resulted in significant propidium iodide staining. Twenty minutes of simulated ischemia, followed by 20 or 60 min of simulated reperfusion, resulted in 8–10% of myocytes staining positive for annexin V. Annexin V-positive cells retained both rod-shaped morphology and contractile function but exhibited the decreased cell width indicative of cell shrinkage. Baseline mitochondrial free Ca2+(111 ± 14 nM) was elevated in reperfused annexin V-negative cells (214 ± 22 nM), and further elevated in annexin V-positive myocytes (382 ± 9 nM). After 60 min of simulated reperfusion, caspase-3-like activity was observed in ∼3% of myocytes, which had a rounded appearance and membrane blebs. These results suggest that the use of annexin V after simulated ischemia-reperfusion uncovers a population of cardiomyocytes whose characteristics appear to be consistent with cells undergoing apoptosis.

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