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

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.

Ethyl acetate extract of Nepenthes adrianii x clipeata induces antiproliferation, apoptosis, and DNA damage against oral cancer cells through oxidative stress

2019 ◽  
Vol 34 (8) ◽  
pp. 891-901 ◽  
Author(s):  
Jen‐Yang Tang ◽  
Sheng‐Yao Peng ◽  
Yuan‐Bin Cheng ◽  
Chun‐Lin Wang ◽  
Ammad Ahmad Farooqi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Oral Cancer ◽  
Ethyl Acetate ◽  
Cancer Cells ◽  
Ethyl Acetate Extract ◽  
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

scholarly journals Methanol Extract of Usnea barbata Induces Cell Killing, Apoptosis, and DNA Damage against Oral Cancer Cells through Oxidative Stress

Antioxidants ◽  
2020 ◽  
Vol 9 (8) ◽  
pp. 694
Author(s):  
Jen-Yang Tang ◽  
Kuang-Han Wu ◽  
Yen-Yun Wang ◽  
Ammad Ahmad Farooqi ◽  
Hurng-Wern Huang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Oral Cancer ◽  
Cancer Cells ◽  
Cell Lines ◽  
Time Course ◽  
Cell Killing ◽  
Parp Cleavage ◽  
Flow Cytometric ◽  
Oral Cancer Cells

Some lichens provide the resources of common traditional medicines and show anticancer effects. However, the anticancer effect of Usnproliea barbata (U. barbata) is rarely investigated, especially for oral cancer cells. The aim of this study was to investigate the cell killing function of methanol extracts of U. barbata (MEUB) against oral cancer cells. MEUB shows preferential killing against a number of oral cancer cell lines (Ca9-22, OECM-1, CAL 27, HSC3, and SCC9) but rarely affects normal oral cell lines (HGF-1). Ca9-22 and OECM-1 cells display the highest sensitivity to MEUB and were chosen for concentration effect and time course experiments to address its cytotoxic mechanisms. MEUB induces apoptosis of oral cancer cells in terms of the findings from flow cytometric assays and Western blotting, such as subG1 accumulation, annexin V detection, and pancaspase activation as well as poly (ADP-ribose) polymerase (PARP) cleavage. MEUB induces oxidative stress and DNA damage of oral cancer cells following flow cytometric assays, such as reactive oxygen species (ROS)/mitochondrial superoxide (MitoSOX) production, mitochondrial membrane potential (MMP) depletion as well as overexpression of γH2AX and 8-oxo-2′deoxyguanosine (8-oxodG). All MEUB-induced changes in oral cancer cells were triggered by oxidative stress which was validated by pretreatment with antioxidant N-acetylcysteine (NAC). In conclusion, MEUB causes preferential killing of oral cancer cells and is associated with oxidative stress, apoptosis, and DNA damage.

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 Withaferin A Induces Oxidative Stress-Mediated Apoptosis and DNA Damage in Oral Cancer Cells

2017 ◽  
Vol 8 ◽  
Author(s):  
Hsueh-Wei Chang ◽  
Ruei-Nian Li ◽  
Hui-Ru Wang ◽  
Jing-Ru Liu ◽  
Jen-Yang Tang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Oral Cancer ◽  
Cancer Cells ◽  
Withaferin A ◽  
Oral Cancer Cells

scholarly journals Manoalide Preferentially Provides Antiproliferation of Oral Cancer Cells by Oxidative Stress-Mediated Apoptosis and DNA Damage

Cancers ◽  
2019 ◽  
Vol 11 (9) ◽  
pp. 1303 ◽  
Author(s):  
Hui-Ru Wang ◽  
Jen-Yang Tang ◽  
Yen-Yun Wang ◽  
Ammad Ahmad Farooqi ◽  
Ching-Yu Yen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Oral Cancer ◽  
Cancer Cells ◽  
Annexin V ◽  
Cancer Drug ◽  
Dna Damages ◽  
Atp Production ◽  
Oral Cancer Cells ◽  
Stress Dependent

Marine sponge-derived manoalide has a potent anti-inflammatory effect, but its potential application as an anti-cancer drug has not yet been extensively investigated. The purpose of this study is to evaluate the antiproliferative effects of manoalide on oral cancer cells. MTS assay at 24 h showed that manoalide inhibited the proliferation of six types of oral cancer cell lines (SCC9, HSC3, OC2, OECM-1, Ca9-22, and CAL 27) but did not affect the proliferation of normal oral cell line (human gingival fibroblasts (HGF-1)). Manoalide also inhibits the ATP production from 3D sphere formation of Ca9-22 and CAL 27 cells. Mechanically, manoalide induces subG1 accumulation in oral cancer cells. Manoalide also induces more annexin V expression in oral cancer Ca9-22 and CAL 27 cells than that of HGF-1 cells. Manoalide induces activation of caspase 3 (Cas 3), which is a hallmark of apoptosis in oral cancer cells, Ca9-22 and CAL 27. Inhibitors of Cas 8 and Cas 9 suppress manoalide-induced Cas 3 activation. Manoalide induces higher reactive oxygen species (ROS) productions in Ca9-22 and CAL 27 cells than in HGF-1 cells. This oxidative stress induction by manoalide is further supported by mitochondrial superoxide (MitoSOX) production and mitochondrial membrane potential (MitoMP) destruction in oral cancer cells. Subsequently, manoalide-induced oxidative stress leads to DNA damages, such as γH2AX and 8-oxo-2’-deoxyguanosine (8-oxodG), in oral cancer cells. Effects, such as enhanced antiproliferation, apoptosis, oxidative stress, and DNA damage, in manoalide-treated oral cancer cells were suppressed by inhibitors of oxidative stress or apoptosis, or both, such as N-acetylcysteine (NAC) and Z-VAD-FMK (Z-VAD). Moreover, mitochondria-targeted superoxide inhibitor MitoTEMPO suppresses manoalide-induced MitoSOX generation and γH2AX/8-oxodG DNA damages. This study validates the preferential antiproliferation effect of manoalide and explores the oxidative stress-dependent mechanisms in anti-oral cancer treatment.

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 Growth Inhibition and Apoptosis-Inducing Effects of Cudraflavone B in Human Oral Cancer Cells via MAPK, NF-κB, and SIRT1 Signaling Pathway

Planta Medica ◽  
2013 ◽  
Vol 79 (14) ◽  
pp. E3-E3
Author(s):  
Hwa-Jeong Lee ◽  
Q-Schick Auh ◽  
Young-Man Lee ◽  
Soo-Kyung Kang ◽  
Seok-Woo Chang ◽  
...  
Keyword(s):  
Oral Cancer ◽  
Growth Inhibition ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Oral Cancer Cells
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