Sandensolide Induces Oxidative Stress-Mediated Apoptosis in Oral Cancer Cells and in Zebrafish Xenograft Model

Presently, natural sources and herbs are being sought for the treatment of human oral squamous cell carcinoma (OSCC) in order to alleviate the side effects of chemotherapy. This study investigates the effect of sandensolide, a cembrane isolated from Sinularia flexibilis, to inhibit human OSCC cell growth with the aim of developing a new drug for the treatment of oral cancer. In vitro cultured human OSCC models (Ca9.22, SCC9 and HSC-3 cell lines) and oral normal cells (HGF-1), as well as a zebrafish xenograft model, were used to test the cytotoxicity of sandensolide (MTT assay), as well as to perform cell cycle analysis and Western blotting. Both the in vitro bioassay and the zebrafish xenograft model demonstrated the anti-oral cancer effect of sandensolide. Moreover, sandensolide was able to significantly suppress colony formation and induce apoptosis, as well as cell cycle arrest, in OSCC by regulating multiple key proteins. Induction of reactive oxygen species (ROS) was observed in sandensolide-treated oral cancer cells. However, these apoptotic changes were rescued by NAC pretreatment. These findings contribute to the knowledge of the model of action of sandensolide, which may induce oxidative stress-mediated cell death pathways as a potential agent in oral cancer therapeutics.

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Sensory acceptable equivalent doses of β-phenylethyl isothiocyanate (PEITC) induce cell cycle arrest and retard the growth of p53 mutated oral cancer in vitro and in vivo

Food & Function ◽

10.1039/c8fo00865e ◽

2018 ◽

Vol 9 (7) ◽

pp. 3640-3656 ◽

Cited By ~ 3

Author(s):

Aroonwan Lam-ubol ◽

Alison Lea Fitzgerald ◽

Arnat Ritdej ◽

Tawaree Phonyiam ◽

Hui Zhang ◽

...

Keyword(s):

Cell Cycle ◽

Oral Cancer ◽

Cell Cycle Arrest ◽

Cancer Cells ◽

Induce Cell Cycle Arrest ◽

Cycle Arrest ◽

Oral Cancer Cells ◽

Phenylethyl Isothiocyanate

Sensory acceptable doses of PEITC are selectively toxic to oral cancer cells via ROS-mediated cell cycle arrest.

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Costunolide Induces Apoptosis via the Reactive Oxygen Species and Protein Kinase B Pathway in Oral Cancer Cells

International Journal of Molecular Sciences ◽

10.3390/ijms22147509 ◽

2021 ◽

Vol 22 (14) ◽

pp. 7509

Author(s):

Hai Huang ◽

Jun-Koo Yi ◽

Su-Geun Lim ◽

Sijun Park ◽

Haibo Zhang ◽

...

Keyword(s):

Reactive Oxygen Species ◽

Cell Cycle ◽

Flow Cytometry ◽

Oral Cancer ◽

Cancer Cells ◽

Reactive Oxygen ◽

Migration And Invasion ◽

Oxygen Species ◽

Oral Cancer Cells

Oral cancer (OC) has been attracted research attention in recent years as result of its high morbidity and mortality. Costunolide (CTD) possesses potential anticancer and bioactive abilities that have been confirmed in several types of cancers. However, its effects on oral cancer remain unclear. This study investigated the potential anticancer ability and underlying mechanisms of CTD in OC in vivo and in vitro. Cell viability and anchorage-independent colony formation assays were performed to examine the antigrowth effects of CTD on OC cells; assessments for migration and invasion of OC cells were conducted by transwell; Cell cycle and apoptosis were investigated by flow cytometry and verified by immunoblotting. The results revealed that CTD suppressed the proliferation, migration and invasion of oral cancer cells effectively and induced cell cycle arrest and apoptosis; regarding the mechanism, CTD bound to AKT directly by binding assay and repressed AKT activities through kinase assay, which thereby downregulating the downstream of AKT. Furthermore, CTD remarkably promotes the generation of reactive oxygen species by flow cytometry assay, leading to cell apoptosis. Notably, CTD strongly suppresses cell-derived xenograft OC tumor growth in an in vivo mouse model. In conclusion, our results suggested that costunolide might prevent progression of OC and promise to be a novel AKT inhibitor.

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Hypoxia Induces Resistance to 5-Fluorouracil in Oral Cancer Cells Via G1 Phase Cell Cycle Arrest

New Trends in the Molecular and Biological Basis for Clinical Oncology ◽

10.1007/978-4-431-88663-1_19 ◽

2009 ◽

pp. 184-190

Author(s):

Sayaka Yoshiba ◽

Daisuke Ito ◽

Tatsuhito Nagumo ◽

Tatsuo Shirota ◽

Masashi Hatori ◽

...

Keyword(s):

Cell Cycle ◽

Oral Cancer ◽

Cell Cycle Arrest ◽

Cancer Cells ◽

Phase Cell ◽

G1 Phase ◽

Cycle Arrest ◽

Oral Cancer Cells

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Mechanism for bone invasion of oral cancer cells mediated by interleukin‐6 in vitro and in vivo

Cancer ◽

10.1002/1097-0142(20001101)89:9<1966::aid-cncr13>3.0.co;2-r ◽

2000 ◽

Vol 89 (9) ◽

pp. 1966-1975 ◽

Cited By ~ 36

Author(s):

Masato Okamoto ◽

Kenji Hiura ◽

Go Ohe ◽

Yasuo Ohba ◽

Kunihoro Terai ◽

...

Keyword(s):

Oral Cancer ◽

Cancer Cells ◽

Interleukin 6 ◽

Bone Invasion ◽

Oral Cancer Cells

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

Antioxidants ◽

10.3390/antiox9080694 ◽

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.

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