scholarly journals Erratum to “Involvement of Nrf2-Mediated Upregulation of Heme Oxygenase-1 in Mollugin-Induced Growth Inhibition and Apoptosis in Human Oral Cancer Cells”

2014 ◽  
Vol 2014 ◽  
pp. 1-3
Author(s):  
Young-Man Lee ◽  
Q-Schick Auh ◽  
Deok-Won Lee ◽  
Jun-Yeol Kim ◽  
Ha-Jin Jung ◽  
...  
Keyword(s):  
Oral Cancer ◽  
Growth Inhibition ◽  
Cancer Cells ◽  
Heme Oxygenase ◽  
Heme Oxygenase 1 ◽  
Oral Cancer Cells

Isoliquiritigenin 2′-methyl ether induces growth inhibition and apoptosis in oral cancer cells via heme oxygenase-1

2010 ◽  
Vol 24 (3) ◽  
pp. 776-782 ◽  
Author(s):  
Young-Man Lee ◽  
Gil-Saeng Jeong ◽  
Hyun-Dae Lim ◽  
Ren-Bo An ◽  
Youn-Chul Kim ◽  
...  
Keyword(s):  
Oral Cancer ◽  
Growth Inhibition ◽  
Cancer Cells ◽  
Heme Oxygenase ◽  
Methyl Ether ◽  
Heme Oxygenase 1 ◽  
Oral Cancer Cells

scholarly journals Erratum to “Isocudraxanthone K Induces Growth Inhibition and Apoptosis in Oral Cancer Cells via Hypoxia Inducible Factor-1α”

2020 ◽  
Vol 2020 ◽  
pp. 1-3
Author(s):  
Mee-Ran Shin ◽  
Hwa-Jeong Lee ◽  
Soo-Kyung Kang ◽  
Q-Schick Auh ◽  
Young-Man Lee ◽  
...  
Keyword(s):  
Oral Cancer ◽  
Growth Inhibition ◽  
Cancer Cells ◽  
Hypoxia Inducible Factor ◽  
Hypoxia Inducible Factor 1Α ◽  
Oral Cancer Cells

Effects of artemisinin and its derivatives on growth inhibition and apoptosis of oral cancer cells

Head & Neck ◽  
2007 ◽  
Vol 29 (4) ◽  
pp. 335-340 ◽  
Author(s):  
Woong Nam ◽  
Jungae Tak ◽  
Ju-Kyoung Ryu ◽  
Mankil Jung ◽  
Jong-In Yook ◽  
...  
Keyword(s):  
Oral Cancer ◽  
Growth Inhibition ◽  
Cancer Cells ◽  
Oral Cancer Cells

scholarly journals Soft Coral-Derived Dihydrosinularin Exhibits Antiproliferative Effects Associated with Apoptosis and DNA Damage in Oral Cancer Cells

2021 ◽  
Vol 14 (10) ◽  
pp. 994
Author(s):  
Kun-Han Yang ◽  
Yu-Sheng Lin ◽  
Sheng-Chieh Wang ◽  
Min-Yu Lee ◽  
Jen-Yang Tang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Cell Growth ◽  
Oral Cancer ◽  
Growth Inhibition ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Soft Coral ◽  
Oral Cancer Cells

Dihydrosinularin (DHS) is an analog of soft coral-derived sinularin; however, the anticancer effects and mechanisms of DHS have seldom been reported. This investigation examined the antiproliferation ability and mechanisms of DHS on oral cancer cells. In a cell viability assay, DHS showed growth inhibition against several types of oral cancer cell lines (Ca9-22, SCC-9, OECM-1, CAL 27, OC-2, and HSC-3) with no cytotoxic side effects on non-malignant oral cells (HGF-1). Ca9-22 and SCC-9 cell lines showing high susceptibility to DHS were selected to explore the antiproliferation mechanisms of DHS. DHS also causes apoptosis as detected by annexin V, pancaspase, and caspase 3 activation. DHS induces oxidative stress, leading to the generation of reactive oxygen species (ROS)/mitochondrial superoxide (MitoSOX) and mitochondrial membrane potential (MitoMP) depletion. DHS also induced DNA damage by probing γH2AX phosphorylation. Pretreatment with the ROS scavenger N-acetylcysteine (NAC) can partly counter these DHS-induced changes. We report that the marine natural product DHS can inhibit the cell growth of oral cancer cells. Exploring the mechanisms of this cancer cell growth inhibition, we demonstrate the prominent role DHS plays in oxidative stress.

scholarly journals FLLL32 Triggers Caspase-Mediated Apoptotic Cell Death in Human Oral Cancer Cells by Regulating the p38 Pathway

2021 ◽  
Vol 22 (21) ◽  
pp. 11860
Author(s):  
Chun-Wen Su ◽  
Chun-Yi Chuang ◽  
Yi-Tzu Chen ◽  
Wei-En Yang ◽  
Yi-Ping Pan ◽  
...  
Keyword(s):  
Oral Cancer ◽  
Cancer Cells ◽  
Molecular Mechanisms ◽  
Caspase 3 ◽  
Apoptotic Cell ◽  
Mapk Signaling ◽  
Heme Oxygenase 1 ◽  
Synthetic Analog ◽  
Oral Cancer Cells ◽  
P38 Pathway

Oral cancer is the most common oral malignant tumor in Taiwan. Although there exist several methods for treatment, oral cancer still has a poor prognosis and high recurrence. FLLL32, a synthetic analog of curcumin with antitumor activity, is currently known to induce melanoma apoptosis and inhibit tumor growth in various cancers. However, few studies have examined the mechanisms of FLLL32 in oral cancer. In this study, we explore whether FLLL32 induces apoptosis in oral cancer. We determined that FLLL32 can inhibit the cell viability of oral cancer. Next, we analyzed the effect of FLLL32 on the cell cycle of oral cancer cells and observed that the proportion of cells in the G2/M phase was increased. Additionally, annexin-V/PI double staining revealed that FLLL32 induced apoptosis in oral cancer cells. Data from the Human Apoptosis Array revealed that FLLL32 increases the expression of cleaved caspase-3 and heme oxygenase-1 (HO-1). FLLL32 activates proteins such as caspase-8, caspase-9, caspase-3, PARP, and mitogen-activated protein kinases (MAPKs) in apoptosis-related molecular mechanisms. Moreover, by using MAPK inhibitors, we suggest that FLLL32 induces the apoptosis of oral cancer cells through the p38 MAPK signaling pathway. In conclusion, our findings suggest that FLLL32 is a potential therapeutic agent for oral cancer by inducing caspase-dependent apoptosis and HO-1 activation through the p38 pathway. We believe that the activation of HO-1 and the p38 pathway by FLLL32 represent potential targets for further research in oral cancer.

scholarly journals Low Concentration of Withaferin a Inhibits Oxidative Stress-Mediated Migration and Invasion in Oral Cancer Cells

Biomolecules ◽  
2020 ◽  
Vol 10 (5) ◽  
pp. 777 ◽  
Author(s):  
Tzu-Jung Yu ◽  
Jen-Yang Tang ◽  
Fu Ou-Yang ◽  
Yen-Yun Wang ◽  
Shyng-Shiou F. Yuan ◽  
...  
Keyword(s):  
Cell Migration ◽  
Oral Cancer ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Withaferin A ◽  
Migration And Invasion ◽  
Heme Oxygenase 1 ◽  
Antioxidant Genes ◽  
Low Concentration ◽  
Oral Cancer Cells

Withaferin A (WFA) has been reported to inhibit cancer cell proliferation based on high cytotoxic concentrations. However, the low cytotoxic effect of WFA in regulating cancer cell migration is rarely investigated. The purpose of this study is to investigate the changes in migration and mechanisms of oral cancer Ca9-22 cells after low concentrations of WFA treatment. WFA under 0.5 μM at 24 h treatment shows no cytotoxicity to oral cancer Ca9-22 cells (~95% viability). Under this condition, WFA triggers reactive oxygen species (ROS) production and inhibits 2D (wound healing) and 3D cell migration (transwell) and Matrigel invasion. Mechanically, WFA inhibits matrix metalloproteinase (MMP)-2 and MMP-9 activities but induces mRNA expression for a group of antioxidant genes, such as nuclear factor, erythroid 2-like 2 (NFE2L2), heme oxygenase 1 (HMOX1), glutathione-disulfide reductase (GSR), and NAD(P)H quinone dehydrogenase 1 (NQO1)) in Ca9-22 cells. Moreover, WFA induces mild phosphorylation of the mitogen-activated protein kinase (MAPK) family, including extracellular signal-regulated kinases 1/2 (ERK1/2), c-Jun N-terminal kinase (JNK), and p38 expression. All WFA-induced changes were suppressed by the presence of ROS scavenger N-acetylcysteine (NAC). Therefore, these results suggest that low concentration of WFA retains potent ROS-mediated anti-migration and -invasion abilities for oral cancer cells.

Methylantcinate A induces tumor specific growth inhibition in oral cancer cells via Bax-mediated mitochondrial apoptotic pathway

2010 ◽  
Vol 20 (20) ◽  
pp. 6145-6148 ◽  
Author(s):  
Wan-Chi Tsai ◽  
Yerra Koteswara Rao ◽  
Shih-Shen Lin ◽  
Ming-Yung Chou ◽  
Yi-Ting Shen ◽  
...  
Keyword(s):  
Oral Cancer ◽  
Growth Inhibition ◽  
Cancer Cells ◽  
Specific Growth ◽  
Apoptotic Pathway ◽  
Mitochondrial Apoptotic Pathway ◽  
Oral Cancer Cells

scholarly journals Ethyl acetate extracts of Nepenthes ventricosa x sibuyanensis leaves cause growth inhibition against oral cancer cells via oxidative stress

2019 ◽  
Vol Volume 12 ◽  
pp. 5227-5239
Author(s):  
Jen-Yang Tang ◽  
Tzu-Jung Yu ◽  
Li-Ching Lin ◽  
Sheng-Yao Peng ◽  
Chun-Lin Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Oral Cancer ◽  
Growth Inhibition ◽  
Ethyl Acetate ◽  
Cancer Cells ◽  
Oral Cancer Cells ◽  
Ethyl Acetate Extracts
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