scholarly journals Pomegranate Extract (POMx) Induces Mitochondrial Dysfunction and Apoptosis of Oral Cancer Cells

Antioxidants ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1117
Author(s):  
Sheng-Yao Peng ◽  
Li-Ching Lin ◽  
Shu-Rong Chen ◽  
Ammad A. Farooqi ◽  
Yuan-Bin Cheng ◽  
...  
Keyword(s):  
Dna Damage ◽  
Mitochondrial Dna ◽  
Oral Cancer ◽  
Cancer Cells ◽  
Cell Lines ◽  
Atp Depletion ◽  
Mitochondrial Dna Copy Number ◽  
Polyphenolic Extract ◽  
Oral Cancer Cells ◽  
Gene Mrna

The anticancer effect of pomegranate polyphenolic extract POMx in oral cancer cells has rarely been explored, especially where its impact on mitochondrial functioning is concerned. Here, we attempt to evaluate the proliferation modulating function and mechanism of POMx against human oral cancer (Ca9-22, HSC-3, and OC-2) cells. POMx induced ATP depletion, subG1 accumulation, and annexin V/Western blotting-detected apoptosis in these three oral cancer cell lines but showed no toxicity to normal oral cell lines (HGF-1). POMx triggered mitochondrial membrane potential (MitoMP) disruption and mitochondrial superoxide (MitoSOX) generation associated with the differential downregulation of several antioxidant gene mRNA/protein expressions in oral cancer cells. POMx downregulated mitochondrial mass, mitochondrial DNA copy number, and mitochondrial biogenesis gene mRNA/protein expression in oral cancer cells. Moreover, POMx induced both PCR-based mitochondrial DNA damage and γH2AX-detected nuclear DNA damage in oral cancer cells. In conclusion, POMx provides antiproliferation and apoptosis of oral cancer cells through mechanisms of mitochondrial impairment.

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.

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 Oxidative Stress-Dependent Synergistic Antiproliferation, Apoptosis, and DNA Damage of Ultraviolet-C and Coral-Derived Sinularin Combined Treatment for Oral Cancer Cells

Cancers ◽  
2021 ◽  
Vol 13 (10) ◽  
pp. 2450
Author(s):  
Sheng-Yao Peng ◽  
Jen-Yang Tang ◽  
Ruei-Nian Li ◽  
Hurng-Wern Huang ◽  
Chang-Yi Wu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Oral Cancer ◽  
Cancer Cells ◽  
Cell Lines ◽  
Combined Treatment ◽  
Ultraviolet C ◽  
Oral Cancer Cells ◽  
Stress Dependent ◽  
Oral Cells

Combined treatment is increasingly used to improve cancer therapy. Non-ionizing radiation ultraviolet-C (UVC) and sinularin, a coral Sinularia flexibilis-derived cembranolide, were separately reported to provide an antiproliferation function to some kinds of cancer cells. However, an antiproliferation function using the combined treatment of UVC/sinularin has not been investigated as yet. This study aimed to examine the combined antiproliferation function and explore the combination of UVC/sinularin in oral cancer cells compared to normal oral cells. Regarding cell viability, UVC/sinularin displays the synergistic and selective killing of two oral cancer cell lines, but remains non-effective for normal oral cell lines compared to treatments in terms of MTS and ATP assays. In tests using the flow cytometry, luminescence, and Western blotting methods, UVC/sinularin-treated oral cancer cells exhibited higher reactive oxygen species production, mitochondrial superoxide generation, mitochondrial membrane potential destruction, annexin V, pan-caspase, caspase 3/7, and cleaved-poly (ADP-ribose) polymerase expressions than that in normal oral cells. Accordingly, oxidative stress and apoptosis are highly induced in a combined UVC/sinularin treatment. Moreover, UVC/sinularin treatment provides higher G2/M arrest and γH2AX/8-hydroxyl-2′deoxyguanosine-detected DNA damages in oral cancer cells than in the separate treatments. A pretreatment can revert all of these changes of UVC/sinularin treatment with the antioxidant N-acetylcysteine. Taken together, UVC/sinularin acting upon oral cancer cells exhibits a synergistic and selective antiproliferation ability involving oxidative stress-dependent apoptosis and cellular DNA damage with low toxic side effects on normal oral cells.

scholarly journals MicroRNA-143 suppresses oral squamous cell carcinoma cell growth, invasion and glucose metabolism through targeting hexokinase 2

2017 ◽  
Vol 37 (3) ◽  
Author(s):  
Xianghui Sun ◽  
Lei Zhang
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Migration ◽  
Glucose Metabolism ◽  
Oral Cancer ◽  
Tumor Suppressor ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Cancer Cells ◽  
Cell Lines ◽  
Oral Cancer Cells

miRNAs are non-coding RNAs that have functions to regulate gene expression and play essential roles in a variety of biological processes of cancers. In the present study, we report miR-143 acts as a tumor suppressor in human oral squamous cell carcinoma (OSCC). The expressions of miR-143 are down-regulated in both OSCC cell lines and patient samples compared with normal adjacent tissues. We found overexpression of miR-143 in oral cancer cell lines suppresses cell migration, cellular glucose metabolism and proliferation. Moreover, overexpression of miR-143 promoted apoptosis and significantly caused cell cycle arrest at G1 stage. The colony formation of oral cancer cells was also suppressed by miR-143. We identified hexokinase 2 (HK2) as a direct target of miR-143 in oral cancer cells. Our data show that miR-143 complementary pairs to the 3′-UTR of HK2 in oral cancer cells, leading to the inhibition of glycolysis in vitro and in vivo. Moreover, knockdown of HK2 by siRNA in oral cancer cells inhibited glucose metabolism, proliferation and migration. Recovery of glucose metabolism by overexpression of HK2 in miR-143 overexpressing cells restores the cell migration and proliferation, suggesting that the miR-143-mediated cancer suppression is through the direct inhibition of HK2. In summary, the present studies highlight miR-143 as a tumor suppressor in OSCC by the suppression of cell migration, glucose metabolism and proliferation through directly targeting HK2, rendering miR-143 a therapeutic strategy for the treatment of clinical OSCC patients.

4β-Hydroxywithanolide E selectively induces oxidative DNA damage for selective killing of oral cancer cells

2017 ◽  
Vol 33 (3) ◽  
pp. 295-304 ◽  
Author(s):  
Jen-Yang Tang ◽  
Hurng-Wern Huang ◽  
Hui-Ru Wang ◽  
Ya-Ching Chan ◽  
Jo-Wen Haung ◽  
...  
Keyword(s):  
Dna Damage ◽  
Oral Cancer ◽  
Cancer Cells ◽  
Oxidative Dna Damage ◽  
Oral Cancer Cells

PARP inhibitor Olaparib Enhances the Apoptotic Potentiality of Curcumin by Increasing the DNA Damage in Oral Cancer Cells through Inhibition of BER Cascade

2019 ◽  
Vol 26 (4) ◽  
pp. 2091-2103 ◽  
Author(s):  
Sefinew Molla ◽  
Krushna Chandra Hembram ◽  
Subhajit Chatterjee ◽  
Deepika Nayak ◽  
Chinmayee Sethy ◽  
...  
Keyword(s):  
Dna Damage ◽  
Oral Cancer ◽  
Cancer Cells ◽  
Parp Inhibitor ◽  
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 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.

Benzyl isothiocyanate promotes apoptosis of oral cancer cells via an acute redox stress-mediated DNA damage response

2016 ◽  
Vol 97 ◽  
pp. 336-345 ◽  
Author(s):  
Yao-Tsung Yeh ◽  
Yen-Nien Hsu ◽  
Sheng-Yun Huang ◽  
Jian-Sheng Lin ◽  
Zi-Feng Chen ◽  
...  
Keyword(s):  
Dna Damage ◽  
Oral Cancer ◽  
Cancer Cells ◽  
Dna Damage Response ◽  
Redox Stress ◽  
Benzyl Isothiocyanate ◽  
Damage Response ◽  
Oral Cancer Cells
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