Effect of Fluoxetine on [Ca^(2+)]i and Cell Viability in OC2 Human Oral Cancer Cells

2014 ◽  
Vol 57 (5) ◽  
pp. 256-264 ◽  
Author(s):  
Ko-Long Lin
Keyword(s):  
Oral Cancer ◽  
Cell Viability ◽  
Cancer Cells ◽  
Oral Cancer Cells

scholarly journals Bufalin Induces Mitochondria-Dependent Apoptosis in Pancreatic and Oral Cancer Cells by Downregulating hTERT Expression via Activation of the JNK/p38 Pathway

2015 ◽  
Vol 2015 ◽  
pp. 1-12 ◽  
Author(s):  
Xin Tian ◽  
Shundong Dai ◽  
Jing Sun ◽  
Shenyi Jiang ◽  
Chengguang Sui ◽  
...  
Keyword(s):  
Dna Damage ◽  
Oral Cancer ◽  
Cell Viability ◽  
Cancer Cells ◽  
P38 Mapk ◽  
Molecular Mechanisms ◽  
Mapk Pathway ◽  
Ros Production ◽  
Oral Cancer Cells ◽  
P38 Pathway

Bufalin, a digoxin-like active component of the traditional Chinese medicine Chan Su, exhibits potent antitumor activities in many human cancers. Bufalin induces mitochondria-dependent apoptosis in cancer cells, but the detailed molecular mechanisms are largely unknown. hTERT, the catalytic subunit of telomerase, protects against mitochondrial damage by binding to mitochondrial DNA and reducing mitochondrial ROS production. In the present study, we investigated the effects of bufalin on the cell viability, ROS production, DNA damage, and apoptosis of CAPAN-2 human pancreatic and CAL-27 human oral cancer cells. Bufalin reduced CAPAN-2 and CAL-27 cell viability with IC50values of 159.2 nM and 122.6 nM, respectively. The reduced cell viability was accompanied by increased ROS production, DNA damage, and apoptosis and decreased expression of hTERT. hTERT silencing in CAPAN-2 and CAL-27 cells by siRNA resulted in increased caspase-9/-3 cleavage and DNA damage and decreased cell viability. Collectively, these data suggest that bufalin downregulates hTERT to induce mitochondria-dependent apoptosis in CAPAN-2 and CAL-27 cells. Moreover, bufalin increased the phosphorylation of JNK and p38-MAPK in CAPAN-2 and CAL-27 cells, and blocking the JNK/p38-MAPK pathway using the JNK inhibitor SP600125 or the p38-MAPK inhibitor SB203580 reversed bufalin-induced hTERT downregulation. Thus, the JNK/p38 pathway is involved in bufalin-induced hTERT downregulation and subsequent induction of apoptosis by the mitochondrial pathway.

scholarly journals Combined Treatment of Sulfonyl Chromen-4-Ones (CHW09) and Ultraviolet-C (UVC) Enhances Proliferation Inhibition, Apoptosis, Oxidative Stress, and DNA Damage against Oral Cancer Cells

2020 ◽  
Vol 21 (17) ◽  
pp. 6443 ◽  
Author(s):  
Sheng-Chieh Wang ◽  
Yen-Yun Wang ◽  
Li-Ching Lin ◽  
Meng-Yang Chang ◽  
Shyng-Shiou F. Yuan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Flow Cytometry ◽  
Dna Damage ◽  
Oral Cancer ◽  
Cell Viability ◽  
Cancer Cells ◽  
Untreated Control ◽  
Combined Treatment ◽  
Proliferation Inhibition ◽  
Oral Cancer Cells

The sensitizing effect of chromone-derived compounds on UVC-induced proliferation inhibition has not been comprehensively investigated so far. The subject of this study was to examine the proliferation change of oral cancer cells while using the combined treatment of UVC (254 nm) with our previously developed sulfonyl chromen-4-ones (CHW09), namely UVC/CHW09. Cell viability, apoptosis, oxidative stress, and DNA damage for the individual and combined treatments for UVC and/or CHW09 were examined in oral cancer Ca9-22 cells. In 24 h MTS assay, UVC (30 J/m2; UVC30), or CHW09 (25 and 50 µg/mL; namely, CHW09-25 and CHW09-50) show 54%, 59%, and 45% viability. The combined treatment (UVC30/CHW09-25 and UVC30/CHW09-50) show lower cell viability (45% and 35%). Mechanistically, UVC/CHW09 induced higher apoptosis than individual treatments and untreated control, which were supported by the evidence of flow cytometry for subG1, annexin V/7-aminoactinomycin D, pancaspase and caspases 3/7 activity, and western blotting for cleaved poly(ADP-ribose) polymerase. Moreover, this cleaved PARP expression was downregulated by pancaspase inhibitor Z-VAD-FMK. UVC/CHW09 showed higher oxidative stress than individual treatments and untreated control in terms of flow cytometry for reactive oxygen species, mitochondrial membrane potential, and mitochondrial mass. Furthermore, UVC/CHW09 showed higher DNA damage than individual treatments and untreated control in terms of flow cytometry for H2A histone family member X and 8-oxo-2’-deoxyguanosine. In conclusion, combined treatment UVC/CHW09 suppresses proliferation, and promotes apoptosis, oxidative stress, and DNA damage against oral cancer cells, providing a novel application of sulfonyl chromen-4-ones in order to sensitize UVC induced proliferation inhibition for oral cancer therapy.

Mechanisms of resveratrol-induced changes in cytosolic free calcium ion concentrations and cell viability in OC2 human oral cancer cells

2014 ◽  
Vol 34 (3) ◽  
pp. 289-299 ◽  
Author(s):  
H-J Chang ◽  
C-T Chou ◽  
H-T Chang ◽  
W-Z Liang ◽  
T-Y Hung ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Oral Cancer ◽  
Cell Viability ◽  
Cancer Cells ◽  
Water Soluble ◽  
Dependent Manner ◽  
Acetoxymethyl Ester ◽  
Fura 2 ◽  
Fluorescence Quench ◽  
Oral Cancer Cells

Resveratrol is a natural compound that affects cellular calcium (Ca2+) homeostasis and viability in different cells. This study examined the effect of resveratrol on cytosolic free Ca2+ concentrations ([Ca2+]i) and viability in OC2 human oral cancer cells. The Ca2+-sensitive fluorescent dye fura-2 was used to measure [Ca2+]i, and water-soluble tetrazolium-1 was used to measure viability. Resveratrol evoked concentration-dependent increase in [Ca2+]i. The response was reduced by removing extracellular Ca2+. Resveratrol also caused manganese-induced fura-2 fluorescence quench. Resveratrol-evoked Ca2+ entry was inhibited by nifedipine and the protein kinase C (PKC) inhibitor GF109203X but was not altered by econazole, SKF96365, and the PKC activator phorbol 12-myristate 13 acetate. In Ca2+-free medium, treatment with the endoplasmic reticulum Ca2+ pump inhibitor 2,5-di- tert-butylhydroquinone (BHQ) abolished resveratrol-evoked [Ca2+]i rise. Conversely, treatment with resveratrol inhibited BHQ-evoked [Ca2+]i rise. Inhibition of phospholipase C (PLC) with U73122 abolished resveratrol-evoked [Ca2+]i rise. At 20–100 μM, resveratrol decreased cell viability, which was not affected by chelating cytosolic Ca2+with 1,2-bis(2-aminophenoxy)ethane- N, N, N′, N′-tetraacetic acid-acetoxymethyl ester. Annexin V-fluorescein isothiocyanate staining data suggest that resveratrol at 20–40 μM induced apoptosis in a concentration-dependent manner. Collectively, in OC2 cells, resveratrol induced [Ca2+]i rise by evoking PLC-dependent Ca2+ release from the endoplasmic reticulum and by causing Ca2+ entry via nifedipine-sensitive, PKC-regulated mechanisms. Resveratrol also caused Ca2+-independent apoptosis.

In Vitro Anticancer Activity of Virgin Coconut Oil and its Fractions in Liver and Oral Cancer Cells

2020 ◽  
Vol 19 (18) ◽  
pp. 2223-2230 ◽  
Author(s):  
Poonam Verma ◽  
Sanjukta Naik ◽  
Pranati Nanda ◽  
Silvi Banerjee ◽  
Satyanarayan Naik ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Oral Cancer ◽  
Anticancer Activity ◽  
Cancer Cells ◽  
Cell Line ◽  
Coconut Oil ◽  
Virgin Coconut Oil ◽  
Anticancer Efficacy ◽  
Oral Cancer Cells

Background: Coconut oil is an edible oil obtained from fresh, mature coconut kernels. Few studies have reported the anticancer role of coconut oil. The fatty acid component of coconut oil directly targets the liver by portal circulation and as chylomicron via lymph. However, the anti-cancer activity of coconut oil against liver cancer cells and oral cancer cells is yet to be tested. The active component of coconut oil, that is responsible for the anticancer activity is not well understood. In this study, three different coconut oils, Virgin Coconut Oil (VCO), Processed Coconut Oil (PCO) and Fractionated Coconut Oil (FCO), were used. Objective: Based on previous studies, it can be hypothesized that fatty acids in coconut oil may have anticancer potential and may trigger cell death in cancer cell lines. Methods: Each cell line was treated with different concentrations of Virgin Coconut Oil (VCO), Processed Coconut Oil (PCO) and Fractionated Coconut Oil (FCO). The treated cells were assayed by MTT after 72 hr of incubation. The fatty acid composition of different coconut oils was analyzed by gas chromatography. Result: Different concentrations of coconut oils were used to treat the cells. Interestingly, the anticancer efficacy of VCO, PCO and FCO was not uniform, rather the efficacy varied from cell line to cell line. Only 20% VCO showed significant anticancer activity in HepG2 cells in comparison to 80% PCO against the KB cell line. Remarkably, 20% of PCO and 5% of FCO showed potential growth inhibition in the KB cell line as compared to 80% PCO in HepG2 cells. Moreover, there was a difference in the efficacy of VCO, PCO and FCO, which might be due to their fatty acid composition. Comparing the anticancer efficacy of VCO, PCO and FCO in this study helped to predict which class of fatty acids and which fatty acid might be associated with the anticancer activity of VCO. Conclusion: This study shows that VCO, PCO and FCO have anticancer efficacy and may be used for the treatment of cancer, especially liver and oral cancer.

Econazole-induced Ca2+ fluxes and apoptosis in human oral cancer cells

2010 ◽  
Vol 71 (4) ◽  
pp. 240-248 ◽  
Author(s):  
Daih-Huang Kuo ◽  
Li-Min Liu ◽  
Hsin-Wei Chen ◽  
Fu-An Chen ◽  
Chung-Ren Jan
Keyword(s):  
Oral Cancer ◽  
Cancer Cells ◽  
Oral Cancer Cells

Effect of the environmental pollutant bisphenol A dimethacylate (BAD) on Ca2+ movement and viability in OC2 human oral cancer cells

2013 ◽  
Vol 35 (2) ◽  
pp. 178-184 ◽  
Author(s):  
Jau-Min Chien ◽  
Chiang-Ting Chou ◽  
Yi-Chau Lu ◽  
Ti Lu ◽  
Chao-Chuan Chi ◽  
...  
Keyword(s):  
Oral Cancer ◽  
Bisphenol A ◽  
Cancer Cells ◽  
Environmental Pollutant ◽  
Oral Cancer Cells

Apoptotic effect of cisplatin and cordycepin on OC3 human oral cancer cells

2013 ◽  
Vol 20 (8) ◽  
pp. 624-632 ◽  
Author(s):  
Ying-hui Chen ◽  
Lyh-Jyh Hao ◽  
Chih-peng Hung ◽  
Jung-wei Chen ◽  
Sew-fen Leu ◽  
...  
Keyword(s):  
Oral Cancer ◽  
Cancer Cells ◽  
Apoptotic Effect ◽  
Oral Cancer Cells

Quercetin Inhibits Proliferation and Drug Resistance in KB/VCR Oral Cancer Cells and Enhances Its Sensitivity to Vincristine

2014 ◽  
Vol 67 (1) ◽  
pp. 126-136 ◽  
Author(s):  
Zhaohu Yuan ◽  
Huili Wang ◽  
Ziyou Hu ◽  
Yanqing Huang ◽  
Fang Yao ◽  
...  
Keyword(s):  
Drug Resistance ◽  
Oral Cancer ◽  
Cancer Cells ◽  
Oral Cancer Cells
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