scholarly journals Interactive effects of 1, 25-dihydroxyvitamin D3 and soy protein extract (SPE) on oral cancer growth in vitro: evidence for potential functional relationships.

2013 ◽  
Vol 3 (6) ◽  
pp. 183 ◽  
Author(s):  
Karl Kingsley ◽  
Mark A. Keiserman ◽  
Christine J. Bergman
Keyword(s):  
Cell Cycle ◽  
Oral Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Vitamin D3 ◽  
Soy Protein ◽  
Interactive Effects ◽  
Protein Extract ◽  
Oral Cancers ◽  
Oral Cancer Cell

Background: Previous studies have found specific soy isoflavones (Genistein, Daidzein, Glycitein) demonstrate anti-tumor properties against several cancer types, including oral cancer. Few studies have evaluated whole soy extract, containing a combination of these isoflavones and other bioreactive compounds, which may function synergistically and more effectively against oral cancers. Preliminary work by this group has now demonstrated whole soy protein extract (SPE) inhibits oral cancer cell growth specifically and selectively, through independent cell-cycle and apoptotic pathways. However, more recent evidence now suggests that ingestion of vitamin D3, either in dietary foods or supplements may potentiate the activity of soy components and their anti-tumor effects.Objective: The primary goal of this study was to investigate the interactive and inter-connected effects of 1, 25-dihydroxyvitamin D3 administration with the anti-proliferative effects of whole soy protein extract (SPE) on oral cancer and normal cell lines in vitro.Methods: Three oral squamous cell carcinoma cell lines (SCC15, SCC25, and CAL27) were treated with 1, 25-dihydroxy Vitamin D3 at physiological concentrations (10-125 nmol). Cell growth was then compared with cell treatment using soy protein extract (SPE) within the normal physiologic range (0 - 10 μM/L). Interactive effects were then evaluated using co-administration of SPE and 1, 25-dihydroxy Vitamin D3. Quantitative RT-PCR was performed at various time points to determine any changes in mRNA expression for key cell cycle and apoptotic signaling pathway regulators, including p53, c-myc, ornithine decarboxylase (ODC), caspase-2, caspase-8, and bax. Results: Administration of 1, 25-dihydroxy Vitamin D3 induced distinct dose-dependent, growth-inhibitory effects in all three oral cancer cell lines examined. These inhibitory effects were comparable to the overall range of growth inhibition induced by SPE. However, the combined effects of co-administration were far greater, suggesting the presence of synergistic relationships between these components. In addition, these results indicate that either treatment alone appeared to modulate mRNA expression of oral cancer cell-cycle promoters c-myc and ODC, as well as the caspase-dependent apoptosis pathway, while only 1, 25-dihydroxy Vitamin D3 administration appeared to influence the bax pathway. Conclusion: These results suggest that co-administration with 1, 25-dihydroxy Vitamin D3 and SPE may enhance their anti-tumor effects. This study may help to explain, in part, why balanced diets rich in fruits, vegetables, and soy protein, are associated with protection against development and progression of oral cancers, although further study is needed to develop specific public health recommendations for oral cancer treatment and prevention.Key words: vitamin D, soy extract, whole soy protein, oral cancer, growth inhibition.

scholarly journals miR-365 (microRNA): Potential Biomarker in Oral Squamous Cell Carcinoma Exosomes and Extracellular Vesicles

2020 ◽  
Vol 21 (15) ◽  
pp. 5317
Author(s):  
Jeffery Coon ◽  
Karl Kingsley ◽  
Katherine M. Howard
Keyword(s):  
Oral Cancer ◽  
Cell Line ◽  
Cell Lines ◽  
Cancer Cell ◽  
Extracellular Vesicles ◽  
Squamous Cell ◽  
Cancer Cell Lines ◽  
Oral Cancers ◽  
Oral Cancer Cell ◽  
Potential Biomarker

Introduction: miR-365 is a non-coding microRNA that regulates transcription and has been demonstrated to promote oncogenesis and metastasis in some cancers, while suppressing these effects in others. Many microRNAs are produced and then exported extracellularly in exosomes, which are small extracellular vesicles ranging from 30 to 100 nm that are found in eukaryotic fluids and facilitate many cellular functions. Exosomes and extracellular vesicles are produced by many cell types, including oral cancer cells—although no study to date has evaluated miR-365 and oral cancer exosomes or extracellular vesicles. Based on this information, our research question was to evaluate whether oral cancers produce exosomes or extracellular vesicles containing miR-365. Materials and Methods: Two commercially available oral cancer cell lines (SCC25 and CAL27) and a normal oral keratinocyte (OKF4) were grown in serum-free media, supplemented with exosome-depleted fetal bovine serum. Extracellular vesicles and exosomes were then isolated using the Invitrogen total exosome RNA and protein isolation kit for processing using the hsa-miR-365a-5p microRNA qPCR assay kit. Results: RNA was successfully isolated from the exosome-depleted supernatant from each cell line—SCC9, SCC15, SCC25, and CAL27 (oral squamous cell carcinomas) and OKF4 (oral epithelial cell line). Relative concentrations of RNA were similar among each cell line, which were not significantly different, p = 0.233. RNA quality was established by A260:A280 absorbance using a NanoDrop, revealing purity ranging 1.73–1.86. Expression of miR-16 was used to confirm the presence of microRNA from the extracted exosomes and extracellular vesicles. The presence of miR-365 was then confirmed and normalized to miR-16 expression, which demonstrated an increased level of miR-365 in both CAL27 and SCC25. In addition, the normalized relative quantity (RQ) for miR-365 exhibited greater variation among SCC25 (1.382–4.363) than CAL27 cells (1.248–1.536). Conclusions: These results confirm that miR-365 is not only expressed in oral cancer cell lines, but also is subsequently exported into exosomes and extracellular vesicles derived from these cultures. These data may help to contextualize the potential for this microRNA to contribute to the phenotypes and behaviors of oral cancers that express this microRNA. Future research will begin to investigate these potential mechanisms and pathways and to determine if miR-365 may be useful as an oral cancer biomarker for salivary or liquid biopsies.

scholarly journals Immunomodulatory Effect and an Intervention of TNF Signalling Leading to Apoptotic and Cell Cycle Arrest on ORL-204 Oral Cancer Cells by Tiger Milk Mushroom, Lignosus rhinocerus

2021 ◽  
Vol 60 (1) ◽  
Author(s):  
Hui Yeng Yeannie Yap ◽  
Boon Hong Kong ◽  
Chee Sum Alvin Yap ◽  
Kien Chai Ong ◽  
Rosnah Binti Zain ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Oral Cancer ◽  
Cell Cycle Arrest ◽  
Cell Lines ◽  
Cancer Cell ◽  
Water Extract ◽  
Cancer Cell Lines ◽  
Phase Cell ◽  
Cycle Arrest ◽  
Oral Cancer Cell

Research background. Tiger milk mushroom (Lignosus rhinocerus) is a medicinal mushroom that is geographically distributed in the region of South China, Thailand, Malaysia, Indonesia, Philippines and Papua New Guinea. Consumption of its sclerotium has been reported to treat various ailments. However, its anticancer potential towards oral cancer cell lines is yet to be discovered considering its traditional method of consumption by biting/chewing of the sclerotium. Experimental approach. Mushroom sclerotial powder of cultivar TM02® was extracted and fractionated by a Sephadex G-50 chromatographic column prior to cytotoxicity testing against a panel of human oral cancer cell lines. The capability of the identified bioactive fraction in regulating several molecules associated with its TNF pathway was investigated. Results and conclusions. MTT proliferation assay indicated that ORL-48 (derived from gingiva), ORL-188 (derived from the tongue), and ORL-204 (derived from buccal mucosa) were inhibited by L. rhinocerus sclerotial cold water extract and its high-molecular-mass fraction (HMM) in varying degree with ORL-204 being most affected. Hence, HMM treatment on ORL-204 was further investigated. HMM induced apoptosis and G0/G1-phase cell cycle arrest through caspase-3/7 cleavage. Activities of MIP2 and COX-2 were downregulated by 0.2- and 4.6-fold respectively in the HMM-treated ORL-204 cells. Novelty and scientific contribution. Using ORL-204, it revealed that HMM may have intervened via the TNF pathway at various network sites in its manifestation as a potential dietary compound for cancer prevention and natural adjunct therapeutic to conventional cancer treatment.

Characterization of URST1 as a prognostic biomarker and therapeutic target for lung and oral cancers.

2017 ◽  
Vol 35 (15_suppl) ◽  
pp. e14057-e14057
Author(s):  
Atsushi Takano ◽  
Yoshihiro Yoshitake ◽  
Masanori Shinohara ◽  
Yohei Miyagi ◽  
Yataro Daigo ◽  
...  
Keyword(s):  
Oral Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Therapeutic Target ◽  
Prognostic Biomarker ◽  
Cancer Cell Lines ◽  
Normal Lung ◽  
Positive Staining ◽  
Oral Cancers ◽  
Oral Cancer Cell

e14057 Background:Lung cancer and oral cavity cancer belong to aerodigestive cancers whose clinical outcome after multimodal therapy remains poor. Methods:To identify new biomarkers and therapeutic targets for lung and oral cancers, we screened genes using our original gene expression profile database for various solid cancers, and characterized clinical and oncogenic values of up-regulated in solid tumor 1 (URST1) protein as a candidate. Results: URST1 was highly expressed in the most of lung or oral cancer cell lines and tumor tissues, but was hardly detected in normal lung or oral epithelial cells and tissues as detected by real-time PCR and western blot analyses. Immunocytochemical analysis revealed that URST1 was mainly localized in the nucleus and cytoplasm of lung or oral cancer cell lines. Immunohistochemical analysis using tissue microarray showed that positive staining of URST1 was observed in 231 of 358 (64.5%) lung cancers, but not in normal lung, and it was significantly associated with poor prognosis after curative surgery. In addition, URST1 was expressed in 64 of 96 (66.7%) oral cancers, but not in oral mucosa, and it was significantly correlated with poor clinical outocome after surgery. Multivariate analysis confirmed that URST1 expression was an independent prognostic factor for oral cancer. Suppression of URST1 expression by siRNA or treatment with synthesized inhibitor specific for URST1 activity inhibited mitosis and growth of lung or oral cancer cell lines. Conclusions:URST1 is likely to be a prognostic biomarker and therapeutic target for aerodigestive cancers such as lung and oral cancers.

Effect of 5-fluorouracil on G1 phase cell cycle regulation in oral cancer cell lines

Oral Oncology ◽  
2004 ◽  
Vol 40 (1) ◽  
pp. 63-70 ◽  
Author(s):  
Ming-Heng Li ◽  
Daisuke Ito ◽  
Misaki Sanada ◽  
Takeshi Odani ◽  
Masashi Hatori ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Oral Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cell Cycle Regulation ◽  
Cancer Cell Lines ◽  
Phase Cell ◽  
G1 Phase ◽  
Oral Cancer Cell ◽  
Cycle Regulation

scholarly journals Assessment of MicroRNA (miR)-365 Effects on Oral Squamous Carcinoma Cell Line Phenotypes

Biomolecules ◽  
2021 ◽  
Vol 11 (6) ◽  
pp. 874
Author(s):  
Jeffrey Coon ◽  
Karl Kingsley
Keyword(s):  
Oral Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Squamous Carcinoma ◽  
Cancer Cell Lines ◽  
Oral Cancers ◽  
Oral Cancer Cell ◽  
Oral Squamous Carcinoma ◽  
Squamous Carcinoma Cell ◽  
Negative Controls

miR-365 is a microRNA that regulates transcription and has been demonstrated to promote oncogenesis and metastasis in some cancers while suppressing these effects in others. Virtually no information is known about the presence or function of miR-365 in oral cancers. Based upon this information, the primary goal of this project was to evaluate the expression of miR-365 in existing oral cancer cell lines. Five commercially available oral cancer cell lines (SCC4, SCC9, SCC15, SCC25, and CAL27) were obtained and cultured. RNA was then screened by PCR using primers specific for miR-365, as well as matrix metalloproteinase (MMP-2) and a downstream cancer stem cell regulator (NKX2.1), and structural and metabolic standards (beta actin, GAPDH). miR-365 was detected among these oral cancers, and some cells also expressed NKX2.1 and MMP-2, which correlated with miR-365 levels. The relative expression of miR-365, NKX2.1, and MMP-2 RNA was higher than expected. Transfection of miR-365 resulted in a significant increase in proliferation, which was not observed in the negative controls. These data appear to confirm miR-365 expression in oral cancers, which may also be correlated with MMP-2 and NKX2.1 expression. Moreover, the fastest growing oral cancers with the highest viability produced the most miR-365. In addition, miR-365 transfected into cells significantly increased growth, even in normal cells. More research is needed to elucidate the pathways responsible for these observations.

scholarly journals PRELIMINARY PHYTOCHEMICAL ANALYSIS AND CYTOTOXICITY POTENTIAL OF PINEAPPLE EXTRACT ON ORAL CANCER CELL LINES

2016 ◽  
pp. 140
Author(s):  
Anirudh Menon ◽  
Vishnu Priya V ◽  
Gayathri R
Keyword(s):  
Oral Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Anticancer Drug ◽  
Cancer Cell Lines ◽  
Phytochemical Analysis ◽  
Phytochemical Composition ◽  
Tetrazolium Bromide ◽  
Oral Cancer Cell ◽  
Natural Way

<p>ABSTRACT<br />Objective: This study aims at performing a preliminary phytochemical analysis to evaluate the phytochemical composition of pineapple extract and<br />its cytotoxicity potential on oral cancer cell lines.<br />Methods: Preliminary phytochemical analysis of pineapple extract was done, 3-(4, 5-Dimethyl-2-thiazolyl)-2, 5-diphenyl-2H-tetrazolium bromide<br />assay for evaluating the cytotoxicity potential of the extract on oral cancer cell lines was performed.<br />Results: Phytoconstituents such as flavonoids, coumarins, and phenols were present in the pineapple extract. The extract also exhibited increased<br />cytotoxicity with increased concentration.<br />Conclusion: This study is conducted to see if pineapple extract is effective in treating oral cancer in a natural way instead of harmful treatments.<br />Keywords: Cytotoxicity, Pineapple extract, Anticancer drug.</p><p> </p>

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