scholarly journals Antitumor Activity of the Cardiac Glycoside αlDiginoside by Modulating Mcl-1 in Human Oral Squamous Cell Carcinoma Cells

2020 ◽  
Vol 21 (21) ◽  
pp. 7947
Author(s):  
Jing-Ru Weng ◽  
Wei-Yu Lin ◽  
Li-Yuan Bai ◽  
Jing-Lan Hu ◽  
Chia-Hsien Feng
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Cardiac Glycoside ◽  
Janus Kinase ◽  
Parp Cleavage ◽  
Diphenyltetrazolium Bromide ◽  
Indigenous Plant ◽  
Induced Apoptosis

We recently isolated a cardiac glycoside (CG), αldiginoside, from an indigenous plant in Taiwan, which exhibits potent tumor-suppressive efficacy in oral squamous cell carcinoma (OSCC) cell lines (SCC2095 and SCC4, IC50 < 0.2 µM; 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assays). Here, we report that αldiginoside caused Sphase arrest and apoptosis, through the inhibition of a series of signaling pathways, including those mediated by cyclin E, phospho-CDC25C (p-CDC25C), and janus kinase/signal transducer and activator of transcription (JAK/STAT)3. αldiginoside induced apoptosis, as indicated by caspase activation and poly (ADP-ribose) polymerase (PARP) cleavage. Equally important, αldiginoside reduced Mcl-1 expression through protein degradation, and overexpression of Mcl-1 partially protected SCC2095 cells from αldiginoside’s cytotoxicity. Taken together, these data suggest the translational potential of αldiginoside to foster new therapeutic strategies for OSCC treatment.

Licochalcone D directly targets JAK2 to induced apoptosis in human oral squamous cell carcinoma

2018 ◽  
Vol 234 (2) ◽  
pp. 1780-1793 ◽  
Author(s):  
Ji-Hye Seo ◽  
Hyun Woo Choi ◽  
Ha-Na Oh ◽  
Mee-Hyun Lee ◽  
Eunae Kim ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Induced Apoptosis

Luteolin Induces Apoptosis in Oral Squamous Cancer Cells

2008 ◽  
Vol 87 (4) ◽  
pp. 401-406 ◽  
Author(s):  
S.-F. Yang ◽  
W.-E. Yang ◽  
H.-R. Chang ◽  
S.-C. Chu ◽  
Y.-S. Hsieh
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Flavonoid Compound ◽  
Caspase 9 ◽  
Continuous Administration ◽  
Apoptotic Protein ◽  
Squamous Cancer ◽  
Induced Apoptosis

Oral squamous cell carcinoma is the most common malignancy of the oral cavity, and treatment approaches are inadequate. Luteolin, a natural flavonoid compound, has been shown to have anti-tumorigenic properties on various types of tumors. Therefore, we hypothesized that luteolin has anti-tumorigenic properties for oral squamous cell carcinoma, and may provide effective chemotherapy. Results revealed that luteolin reduced the viability of SCC-4 cells and induced apoptosis by decreasing the expression of cyclin-dependent kinase (CDKs), cyclins, and phosphor- retinoblastoma (p-Rb) anti-apoptotic protein, but increased the expression of pro-apoptotic proteins and activated caspase 9 and 3, with a concomitant increase in the levels of cleaved poly-ADP-ribose polymerase (PARP). Combination treatment of luteolin with paclitaxel enhanced the cytotoxic effect of paclitaxel in SCC-4 cells, and continuous administration of luteolin suppressed the growth of xenograft tumors in nude mice. These results suggest that luteolin could be an effective chemotherapeutic agent for the treatment of oral squamous cell carcinoma.

scholarly journals Cinobufagin Exerts Anticancer Activity in Oral Squamous Cell Carcinoma Cells through Downregulation of ANO1

2021 ◽  
Vol 22 (21) ◽  
pp. 12037
Author(s):  
Sungwoo Jo ◽  
Eunhee Yang ◽  
Yechan Lee ◽  
Dongkyu Jeon ◽  
Wan Namkung
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Chloride Channel ◽  
Smooth Muscle Contraction ◽  
Parp Cleavage ◽  
Potential Candidate ◽  
Dependent Manner ◽  
Protein Levels

Anoctamin1 (ANO1), a calcium-activated chloride channel, is frequently overexpressed in several cancers, including oral squamous cell carcinoma (OSCC). OSCC is a highly aggressive cancer and the most common oral malignancy. ANO1 has been proposed as a potential candidate for targeted anticancer therapy. In this study, we performed a cell-based screening to identify novel regulators leading to the downregulation of ANO1, and discovered cinobufagin, which downregulated ANO1 expression in oral squamous cell carcinoma CAL-27 cells. ANO1 protein levels were significantly reduced by cinobufagin in a dose-dependent manner with an IC50 value of ~26 nM. Unlike previous ANO1 inhibitors, short-term (≤10 min) exposure to cinobufagin did not alter ANO1 chloride channel activity and ANO1-dependent intestinal smooth muscle contraction, whereas long-term (24 h) exposure to cinobufagin significantly reduced phosphorylation of STAT3 and mRNA expression of ANO1 in CAL-27 cells. Notably, cinobufagin inhibited cell proliferation of CAL-27 cells expressing high levels of ANO1 more potently than that of ANO1 knockout CAL-27 cells. In addition, cinobufagin significantly reduced cell migration and induced caspase-3 activation and PARP cleavage in CAL-27 cells. These results suggest that downregulation of ANO1 by cinobufagin is a potential mechanism for the anticancer effect of cinobufagin in OSCC.

Anti-PD-L1-modified and ATRA-loaded nanoparticles for immuno-treatment of oral dysplasia and oral squamous cell carcinoma

Nanomedicine ◽  
2020 ◽  
Vol 15 (10) ◽  
pp. 951-968 ◽  
Author(s):  
Xiao-Jie Chen ◽  
Xue-Qiong Zhang ◽  
Ming-Xiu Tang ◽  
Qi Liu ◽  
Gang Zhou
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Squamous Carcinoma ◽  
Oral Dysplasia ◽  
Squamous Carcinoma Cells ◽  
Induced Apoptosis

Aim: To develop nanomedicines for immuno-therapy of oral dysplasia and oral squamous cell carcinoma. Materials & methods: All-trans retinoic acid (ATRA)-poly(lactide-co-glycolide acid) (PLGA)-poly(ethylene glycol) (PEG)-programmed death-ligand 1 (PD-L1) nanomedicines were fabricated by loading ATRA into PLGA-PEG nanocarriers and modification using an anti-PD-L1 antibody. Results: ATRA-PLGA-PEG-PD-L1 nanoparticles showed fast cellular uptake, significantly inhibited proliferation and induced apoptosis in DOK and CAL27 cells. Moreover, in C3H tumor-bearing mice, ATRA-PLGA-PEG-PD-L1 nanoparticles more specifically targeted tumor cells, enhanced anticancer activity and reduced side effects when compared with free ATRA. Furthermore, CD8+ T cells were activated around PD-L1 positive cells in the tumor microenvironment after treatment. Conclusion: ATRA-PLGA-PEG-PD-L1 nanoparticles had low toxicity, high biocompatibility and specifically targeted oral dysplasia and squamous carcinoma cells both in vitro and in vivo.

scholarly journals Brucea javanica Leaf Extract Induced Apoptosis in Human Oral Squamous Cell Carcinoma (HSC2) Cells by Attenuation of Mitochondrial Membrane Permeability

2015 ◽  
Vol 7 (2) ◽  
pp. 107
Author(s):  
Britanto Dani Wicaksono ◽  
Enos Tangkearung ◽  
Ferry Sandra
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Membrane Permeability ◽  
Squamous Cell ◽  
Mitochondrial Membrane ◽  
Leaf Extract ◽  
Mitochondrial Membrane Permeability ◽  
Brucea Javanica ◽  
Induced Apoptosis

BACKGROUND: Brucea javanica extract has been reported to have anti-proliferative and cell death induction activities. B. javanica extract was reported to induce apoptosis through caspase cascade. Most of investigated B. javanica extracts were derived from seeds and fruits, or commercially available oil emulsion. Therefore we conducted a study on B. javanica leaf extract (BJLE) in oral cancer cells.METHODS: B. javanica leaves were collected, identified, minced, dried, extracted with distilled ethanol at room temperature for 24 hours, filtered and evaporated. Resulted BJLE was stored at 4°C. Human oral squamous cell carcinoma (HSC)-2 cells were fasted for 12 hours and treated with BJLE in various concentrations for 24 hours. Cells were then quantified with 3-(4,5-dimethylthiazol-2-yl)-2,5-Diphenyltetrazolium bromide (MTT) assay, demonstrated with 4',6'-diamidino-2-phenylindole (DAPI) staining. To find out mitochondrial membrane permeability (MMP), mitochondrial membrane potential (ΔΨM) was analyzed.RESULTS: BJLE reduced percentage of viable HSC-2 cells in a concentration dependent manner. BJLE induced apoptosis in HSC-2 cells. With treatment of 50 μg/ml BJLE, fragmented nuclei were seen. ΔΨM of HSC-2 cells treated with 50 μg/ml BJLE were shifted to the left, meaning that BJLE induced reduction of ΔΨM and attenuation of MMP.CONCLUSION: Our results suggested that BJLE could induce apoptosis by attenuating MMP.KEYWORDS: Brucea javanica, leaf, apoptosis, HSC-2, MTT, DAPI, mitochondria, permeability

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