Activation of Toll-like receptor 3 induces apoptosis of oral squamous carcinoma cells in vitro and in vivo

2012 ◽  
Vol 44 (8) ◽  
pp. 1266-1275 ◽  
Author(s):  
Qingqiong Luo ◽  
Shuiqing Hu ◽  
Ming Yan ◽  
Zujun Sun ◽  
Wantao Chen ◽  
...  
Keyword(s):  
Squamous Carcinoma ◽  
Carcinoma Cells ◽  
Toll Like Receptor ◽  
Squamous Carcinoma Cells ◽  
Oral Squamous Carcinoma

scholarly journals Apoptotic Effects of Diosgeninlactoside on Oral Squamous Carcinoma Cells in Vitro and in Vivo

2014 ◽  
Vol 37 (9) ◽  
pp. 1450-1459 ◽  
Author(s):  
Xu Wang ◽  
Chongkui Sun ◽  
Shiliang He ◽  
Xiurong Guo ◽  
Hao Xu ◽  
...  
Keyword(s):  
Squamous Carcinoma ◽  
Carcinoma Cells ◽  
Squamous Carcinoma Cells ◽  
Oral Squamous Carcinoma ◽  
Apoptotic Effects

scholarly journals Anticancer Effects of Salvia miltiorrhiza Alcohol Extract on Oral Squamous Carcinoma Cells

2017 ◽  
Vol 2017 ◽  
pp. 1-9 ◽  
Author(s):  
Wen-Hung Wang ◽  
Kuo-Yu Hsuan ◽  
Ling-Ya Chu ◽  
Chia-Ying Lee ◽  
Yu-Chang Tyan ◽  
...  
Keyword(s):  
Salvia Miltiorrhiza ◽  
Squamous Carcinoma ◽  
Mitochondrial Pathway ◽  
Carcinoma Cells ◽  
Tumor Xenograft ◽  
Alcohol Extract ◽  
Squamous Carcinoma Cells ◽  
Anticancer Effects ◽  
Oral Squamous Carcinoma

Researchers have reported significant effects from Danshen (Salvia miltiorrhiza) in terms of inhibiting tumor cell proliferation and promoting apoptosis in breast cancer, hepatocellular carcinomas, promyelocytic leukemia, and clear cell ovary carcinomas. Here we report our data indicating that Danshen extracts, especially alcohol extract, significantly inhibited the proliferation of the human oral squamous carcinoma (OSCC) cell lines HSC-3 and OC-2. We also observed that Danshen alcohol extract activated the caspase-3 apoptosis executor by impeding members of the inhibitor of apoptosis (IAP) family, but not by regulating the Bcl-2-triggered mitochondrial pathway in OSCC cells. Our data also indicate that the extract exerted promising effects in vivo, with HSC-3 tumor xenograft growth being suppressed by 40% and 69% following treatment with Danshen alcohol extract at 50 and 100 mg/kg, respectively, for 34 days. Combined, our results indicate appreciable anticancer activity and significant potential for Danshen alcohol extract as a natural antioxidant and herbal human oral cancer chemopreventive drug.

scholarly journals Tumor protein D52 is upregulated in oral squamous carcinoma cells under hypoxia in a hypoxia-inducible-factor-independent manner and is involved in cell death resistance

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Yuzo Abe ◽  
Yoshiki Mukudai ◽  
Mai Kurihara ◽  
Asami Houri ◽  
Junichiro Chikuda ◽  
...  
Keyword(s):  
Hypoxia Inducible Factor ◽  
Squamous Carcinoma ◽  
Cancer Therapeutics ◽  
Tumor Xenograft ◽  
Independent Manner ◽  
Protein Levels ◽  
Squamous Carcinoma Cells ◽  
Oral Squamous Carcinoma

Abstract Background Tumor protein D52 (TPD52) reportedly plays an important role in the proliferation and metastasis of various cancer cells, including oral squamous cell carcinoma (OSCC) cells, and is expressed strongly at the center of the tumor, where the microenvironment is hypoxic. Thus, the present study investigated the roles of TPD52 in the survival and death of OSCC cells under hypoxia, and the relationship with hypoxia-inducible factor (HIF). We examined the expression of TPD52 in OSCC cells under hypoxic conditions and analyzed the effects of HIF on the modulation of TPD52 expression. Finally, the combinational effects of TPD52 knockdown and HIF inhibition were investigated both in vitro and in vivo. Results The mRNA and protein levels of TPD52 increased in OSCC cells under hypoxia. However, the increase was independent of HIF transcription. Importantly, the observation was due to upregulation of mRNA stability by binding of mRNA to T-cell intercellular antigen (TIA) 1 and TIA-related protein (TIAR). Simultaneous knockdown of TPD52 and inhibition of HIF significantly reduced cell viability. In addition, the in vivo tumor-xenograft experiments showed that TPD52 acts as an autophagy inhibitor caused by a decrease in p62. Conclusions This study showed that the expression of TPD52 increases in OSCC cells under hypoxia in a HIF-independent manner and plays an important role in the proliferation and survival of the cells in concordance with HIF, suggesting that novel cancer therapeutics might be led by TPD52 suppression.

scholarly journals Tumor Protein D52 Is Upregulated in Oral Squamous Carcinoma Cells Under Hypoxia in a Hypoxia-inducible-factor-independent Manner and Is Involved in Cell Death Resistance

2021 ◽  
Author(s):  
Yuzo Abe ◽  
Yoshiki Mukudai ◽  
Mai Kurihara ◽  
Asami Houri ◽  
Junichiro Chikuda ◽  
...  
Keyword(s):  
Hypoxia Inducible Factor ◽  
Squamous Carcinoma ◽  
Cancer Therapeutics ◽  
Tumor Xenograft ◽  
Independent Manner ◽  
Protein Levels ◽  
Squamous Carcinoma Cells ◽  
Oral Squamous Carcinoma

Abstract Background. Tumor protein D52 (TPD52) reportedly plays an important role in the proliferation and metastasis of various cancer cells, including oral squamous cell carcinoma (OSCC) cells, and is expressed strongly at the center of the tumor, where the microenvironment is hypoxic. Thus, the present study investigated the roles of TPD52 in the survival and death of OSCC cells under hypoxia, and the relationship with hypoxia-inducible factor (HIF). We examined the expression of TPD52 in OSCC cells under hypoxic conditions and analyzed the effects of HIF on the modulation of TPD52 expression. Finally, the combinational effects of TPD52 knockdown and HIF inhibition were investigated both in vitro and in vivo.Results. The mRNA and protein levels of TPD52 increased in OSCC cells under hypoxia. However, the increase was independent of HIF transcription. Importantly, the observation was due to upregulation of mRNA stability by binding of mRNA to T-cell intercellular antigen (TIA) 1 and TIA-related protein (TIAR). Simultaneous knockdown of TPD52 and inhibition of HIF significantly reduced cell viability. In addition, the in vivo tumor-xenograft experiments showed that TPD52 acts as an autophagy inhibitor caused by a decrease in p62.Conclusions. This study showed that the expression of TPD52 increases in OSCC cells under hypoxia in a HIF-independent manner and plays an important role in the proliferation and survival of the cells in concordance with HIF, suggesting that novel cancer therapeutics might be led by TPD52 suppression.

scholarly journals Doxorubicin metabolism moderately attributes to putative toxicity in prodigiosin/doxorubicin synergism in vitro cells

2020 ◽  
Vol 475 (1-2) ◽  
pp. 119-126
Author(s):  
Shian-Ren Lin ◽  
Chun-Shu Lin ◽  
Ching-Cheng Chen ◽  
Feng-Jen Tseng ◽  
Tsung-Jui Wu ◽  
...  
Keyword(s):  
Squamous Carcinoma ◽  
Human Kidney ◽  
Carcinoma Cells ◽  
Heart Cells ◽  
Slight Reduction ◽  
Normal Cells ◽  
Squamous Carcinoma Cells ◽  
Oral Squamous Carcinoma ◽  
Metabolic Reduction

Abstract Doxorubicin (Dox) is a widely neoplasm chemotherapeutic drug with high incidences of cardiotoxicity. Prodigiosin (PG), a red bacterial pigment from Serratia marcescens, has been demonstrated to potentiate Dox’s cytotoxicity against oral squamous cell carcinoma cells through elevating Dox influx and identified as a Dox enhancer via PG-induced autophagy; however, toxicity of normal cell remains unclear. This study is conducted to evaluate putative cytotoxicity features of PG/Dox synergism in the liver, kidney, and heart cells and further elucidate whether PG augmented Dox’s effect via modulating Dox metabolism in normal cells. Murine hepatocytes FL83B, cardio-myoblast h9c2, and human kidney epithelial cells HK-2 were sequentially treated with PG and Dox by measuring cell viability, cell death characteristics, oxidative stress, Dox flux, and Dox metabolism. PG could slightly significant increase Dox cytotoxicity in all tested normal cells whose toxic alteration was less than that of oral squamous carcinoma cells. The augmentation of Dox cytotoxicity might be attributed to the increase of Dox-mediated ROS accumulation that might cause slight reduction of Dox influx and reduction of Dox metabolism. It was noteworthy to notice that sustained cytotoxicity appeared in normal cells after PG and Dox were removed. Taken together, moderately metabolic reduction of Dox might be ascribed to the mechanism of increase Dox cytotoxicity in PG-induced normal cells; nevertheless, the determination of PG/Dox dose with sustained cytotoxicity in normal cells needs to be comprehensively considered.

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