scholarly journals Manoalide Shows Mutual Interaction between Cellular and Mitochondrial Reactive Species with Apoptosis in Oral Cancer Cells

2021 ◽  
Vol 2021 ◽  
pp. 1-16
Author(s):  
Hui-Ru Wang ◽  
Ping-Ho Chen ◽  
Jen-Yang Tang ◽  
Ching-Yu Yen ◽  
Yong-Chao Su ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Oral Cancer ◽  
Cancer Cells ◽  
Radical Anion ◽  
Annexin V ◽  
Reactive Species ◽  
Fluorescence Staining ◽  
Oral Cancer Cells ◽  
Induced Apoptosis ◽  
Carbonate Radical Anion

We previously found that marine sponge-derived manoalide induced antiproliferation and apoptosis of oral cancer cells as well as reactive species generations probed by dichloro-dihydrofluorescein diacetate (DCFH-DA) and MitoSOX Red. However, the sources of cellular and mitochondrial redox stresses and the mutual interacting effects between these redox stresses and apoptosis remain unclear. To address this issue, we examined a panel of reactive species and used the inhibitors of cellular reactive species (N-acetylcysteine (NAC)), mitochondrial reactive species (MitoTEMPO), and apoptosis (Z-VAD-FMK; ZVAD) to explore their interactions in manoalide-treated oral cancer Ca9-22 and CAL 27 cells. Hydroxyl (˙OH), nitrogen dioxide (NO2˙), nitric oxide (˙NO), carbonate radical-anion (CO3˙–), peroxynitrite (ONOO–), and superoxide (O2˙–) were increased in oral cancer cells following manoalide treatments in terms of fluorescence staining and flow cytometry. Cellular reactive species (˙OH, NO2⋅, ˙NO, CO3˙–, and ONOO–) as well as cellular and mitochondrial reactive species (O2˙–) were induced in oral cancer cells following manoalide treatment for 6 h. NAC, MitoTEMPO, and ZVAD inhibit manoalide-induced apoptosis in terms of annexin V and pancaspase activity assays. Moreover, NAC inhibits mitochondrial reactive species and MitoTEMPO inhibits cellular reactive species, suggesting that cellular and mitochondrial reactive species can crosstalk to regulate each other. ZVAD shows suppressing effects on the generation of both cellular and mitochondrial reactive species. In conclusion, manoalide induces reciprocally activation between cellular and mitochondrial reactive species and apoptosis in oral cancer cells.

scholarly journals Roe Protein Hydrolysates of Giant Grouper (Epinephelus lanceolatus) Inhibit Cell Proliferation of Oral Cancer Cells Involving Apoptosis and Oxidative Stress

2016 ◽  
Vol 2016 ◽  
pp. 1-12 ◽  
Author(s):  
Jing-Iong Yang ◽  
Jen-Yang Tang ◽  
Ya-Sin Liu ◽  
Hui-Ru Wang ◽  
Sheng-Yang Lee ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Oral Cancer ◽  
Cancer Cells ◽  
Annexin V ◽  
Antioxidant Property ◽  
Protein Hydrolysates ◽  
Atp Assay ◽  
Oral Cancer Cells ◽  
Induced Apoptosis ◽  
The Impact

Roe protein hydrolysates were reported to have antioxidant property but the anticancer effects were less addressed, especially for oral cancer. In this study, we firstly used the ultrafiltrated roe hydrolysates (URH) derived from giant grouper (Epinephelus lanceolatus) to evaluate the impact of URH on proliferation against oral cancer cells. We found that URH dose-responsively reduced cell viability of two oral cancer cells (Ca9-22 and CAL 27) in terms of ATP assay. Using flow cytometry, URH-induced apoptosis of Ca9-22 cells was validated by morphological features of apoptosis, sub-G1 accumulation, and annexin V staining in dose-responsive manners. URH also induced oxidative stress in Ca9-22 cells in terms of reactive oxygen species (ROS)/superoxide generations and mitochondrial depolarization. Taken together, these data suggest that URH is a potential natural product for antioral cancer therapy.

scholarly journals Effects of miR-34b/miR-892a Upregulation and Inhibition of ABCB1/ABCB4 on Melatonin-Induced Apoptosis in VCR-Resistant Oral Cancer Cells

2020 ◽  
Vol 19 ◽  
pp. 877-889 ◽  
Author(s):  
Ming-Ju Hsieh ◽  
Chiao-Wen Lin ◽  
Shih-Chi Su ◽  
Russel J. Reiter ◽  
Andy Wei-Ge Chen ◽  
...  
Keyword(s):  
Oral Cancer ◽  
Cancer Cells ◽  
Oral Cancer Cells ◽  
Induced Apoptosis

Sorafenib potentiates ABT-737-induced apoptosis in human oral cancer cells

2017 ◽  
Vol 73 ◽  
pp. 1-6 ◽  
Author(s):  
Lee-Han Kim ◽  
Ji-Ae Shin ◽  
Boonsil Jang ◽  
In-Hyoung Yang ◽  
Dong-Hoon Won ◽  
...  
Keyword(s):  
Oral Cancer ◽  
Cancer Cells ◽  
Oral Cancer Cells ◽  
Induced Apoptosis

scholarly journals Cathepsin B mediates TRAIL-induced apoptosis in oral cancer cells

2005 ◽  
Vol 132 (3) ◽  
pp. 171-183 ◽  
Author(s):  
Nagathihalli S. Nagaraj ◽  
Nadarajah Vigneswaran ◽  
Wolfgang Zacharias
Keyword(s):  
Oral Cancer ◽  
Cancer Cells ◽  
Cathepsin B ◽  
Oral Cancer Cells ◽  
Induced Apoptosis

scholarly journals Effect of thimerosal on Ca2+ movement and viability in human oral cancer cells

2009 ◽  
Vol 28 (5) ◽  
pp. 301-308 ◽  
Author(s):  
LN Kuo ◽  
CJ Huang ◽  
YC Fang ◽  
CC Huang ◽  
JL Wang ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Oral Cancer ◽  
Cancer Cells ◽  
Phospholipase C ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Flow Cytometry Data ◽  
Entry Inhibitors ◽  
Oral Cancer Cells ◽  
Induced Apoptosis

The effect of thimerosal on cytosolic free Ca2+ concentrations ([Ca2+]i ) in human oral cancer cells (OC2) is unclear. This study explored whether thimerosal changed basal [Ca2+]i levels in suspended OC2 cells using fura-2. Thimerosal at concentrations between 1and 50 μM increased [Ca2+]i in a concentration-dependent manner. The Ca2+ signal was reduced partly by removing extracellular Ca 2+. Thimerosal-induced Ca2+ influx was not blocked by L-type Ca2+ entry inhibitors and protein kinase C modulators (phorbol 12-myristate 13-acetate [PMA] and GF109203X). In Ca2+-free medium, 50 μM thimerosal failed to induce a [Ca2+]i rise after pretreatment with thapsigargin (an endoplasmic reticulum Ca2+ pump inhibitor). Inhibition of phospholipase C with U73122 did not change thimerosal-induced [Ca2+]i rises. At concentrations between 5 and 10 μM, thimerosal killed cells in a concentration-dependent manner. The cytotoxic effect of 8 μM thimerosal was potentiated by prechelating cytosolic Ca2+ with the Ca2+ chelator 1,2-bis(2-aminophenoxy)ethane-N,N,N′,N′-tetraacetate/acetomethyl (BAPTA/ AM). Flow cytometry data suggested that 1—7 μM thimerosal-induced apoptosis in a concentration-dependent manner. Collectively, in OC2 cells, thimerosal-induced [Ca2+]i rises by causing phospholipase C-independent Ca2+ release from the endoplasmic reticulum and Ca2+ influx through non—L-type Ca2+ channels. Thimerosal killed cells in a concentration-dependent manner through apoptosis.

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.

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