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 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

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.

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