scholarly journals Remedial Effects and Molecular Docking Studies of Nevadensin: ‎Antiglucosidase, Anti-cholinesterase, and Anti-Human Oral Squamous ‎Cell Carcinoma Potentials

2021 ◽  
Author(s):  
Xu Lan ◽  
Li Liu ◽  
Guangyu Wu
Keyword(s):  
Squamous Cell Carcinoma ◽  
Molecular Docking ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Cell Line ◽  
Cell Lines ◽  
Squamous Cell ◽  
Antioxidant Activities ◽  
Biological Activities ◽  
Radical Scavenging

IntroductionNevadensin has a variety of pharmacological effects, including effects of anti-mycobacterium ‎tuberculosis, antitussive, anti-hypertensive, anti-inflammatory, and free radical-scavenging ‎activities. In this study, we investigated for their anticholinergics, antidiabetic, and anti-‎human oral squamous cell carcinoma potentials for nevadensin. ‎Material and methodsThe antioxidant activities of nevadensin were elucidated by using various bioanalytical assays. ‎On the other hand, IC50 values were calculated for acetylcholine esterase, α-glucosidase ‎inhibition effects of nevadensin. For determining of anti-human oral squamous cell carcinoma ‎properties of nevadensin, MTT assay was used on HUVEC, HSC-3, HSC-4, and Ca9-22 cell ‎lines. The molecular docking method used to compare the biological activities of the ‎nevadensin molecule against enzymes was used. Afterwards, the ADME/T analysis was ‎performed to investigate the drug availability of the nevadensin molecule and the obtained ‎parameters from ADME/T analysis were examined.‎ResultsThe cell viability of nevadensin was very low against human oral squamous cell carcinoma cell ‎lines without any cytotoxicity on the human normal (HUVEC) cell line. The IC50 of the ‎nevadensin against HSC-3, HSC-4, and Ca9-22 were 316, 273, and 399 µg/mL, respectively. ‎Thereby, the best cytotoxicity results and anti-human oral squamous cell carcinoma potentials ‎of our nevadensin was observed in the case of the HSC-4 cell line. ‎ConclusionsMaybe the anti-human lung carcinoma properties of nevadensin are related to their antioxidant ‎effects. ‎

scholarly journals LncRNA NEAT1 mediates progression of oral squamous cell carcinoma via VEGF-A and Notch signaling pathway

2020 ◽  
Vol 18 (1) ◽  
Author(s):  
Ke He ◽  
Zhi-Bin Zhu ◽  
Rui Shu ◽  
Ai Hong
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Notch Signaling ◽  
Cell Carcinoma ◽  
Cell Line ◽  
Signaling Pathway ◽  
Cell Lines ◽  
Squamous Cell ◽  
Notch Signaling Pathway ◽  
Lncrna Neat1

Abstract Background lncRNAs and VEGF have been shown to have close connections with oral squamous cell carcinoma (OSCC). We explored the interaction between lncRNA NEAT1 and VEGF-A in OSCC. Methods RT-qPCR was implemented to measure levels of lncRNA NEAT1 and VEGF-A in OSCC cell lines and normal cell lines. Cell functions then were checked after regulating the expressions of lncRNA NEAT1 and VEGF-A separately. Cell viabilities were examined with CCK-8 and apoptosis rate was checked with flow cytometry. Meanwhile, EMT-related genes E-cadherin, N-cadherin, Vimentin, and Snail and Notch signaling genes Notch1, Notch2, and Jagged were evaluated by RT-qPCR. IMR-1 was applied for impeding Notch signaling pathway. Later, cell viabilities, apoptosis, and EMT were assessed. Results Expressions of lncRNA NEAT1 and VEGF-A were both increased significantly in OSCC cell lines especially in TSCC1 cell line. Suppression of lncNRA NEAT1 was associated with lower cell viabilities and EMT and higher apoptosis rate in the TSCC1 cell line. Meanwhile, knockdown of VEGF-A significantly repressed cell viabilities and EMT in the TSCC1 cell line. Magnifying functions of inhibited lncRNA NEAT1 Notch signaling pathway was obviously activated with overexpressions of lncRNA NEAT1 and VEGF-A. Adding IMR-1 significantly downregulated cell viabilities and EMT and sharply increased apoptosis in the context of lncRNA NEAT1 and VEGF-A overexpression. Conclusion LncRNA NEAT1 may upregulate proliferation and EMT and repress apoptosis through activating VEGF-A and Notch signaling pathway in vitro, suggesting an underlying regulatory factor in OSCC. Nevertheless, further research is necessary to gain a greater understanding of lncRNA NEAT1 and connections with VEGF-A in vivo and in clinical study.

scholarly journals Identification of E2F transcription factor 7 as a novel potential biomarker for oral squamous cell carcinoma

2021 ◽  
Vol 17 (1) ◽  
Author(s):  
Ping Zhou ◽  
Lei Xiao ◽  
Xiaonan Xu
Keyword(s):  
Squamous Cell Carcinoma ◽  
Transcription Factor ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Cell Lines ◽  
Squamous Cell ◽  
Loss Function ◽  
High Expression ◽  
E2f Transcription Factor ◽  
Gain And Loss

Abstract Background As a tumor-accelerating transcriptional factor, E2F transcription factor 7 (E2F7) was up-regulated in many forms of cancers. Nevertheless, little has been reported about the impacts of E2F7 on oral squamous cell carcinoma (OSCC). Here, we aimed to probe whether E2F7 had influences on OSCC and its potential mechanism. Methods The expression of E2F7 in OSCC tissues was analyzed using the data acquired from TCGA and ONCOMINE databases. E2F7 prognostic value in OSCC patients was analyzed utilizing TCGA database. The expression of E2F7 in OSCC cell lines was detected by qRT-PCR. Gain-and loss-function of E2F7 assays in TCA-83 and CAL27 cells were performed respectively to inquire the function of E2F7. Western blotting was applied to test the alternations of EMT-related markers. Results In OSCC tissues, E2F7 was highly expressed. Besides, high expression of E2F7 predicted worse prognosis in OSCC patients. Moreover, E2F7 was over-expressed in TCA-83, HSC-4 and CAL27 (all OSCC cell lines) cells relative to that in HNOK (a normal cell line) cells. Gain-and loss-function assays displayed that deficiency of E2F7 suppresses CAL27 cell growth, migration, invasion and E2F7 high-expression resulted in inverse outcomes in TCA-83 cells. Finally, we found that silencing of E2F7 facilitated E-cadherin protein expression level and reduced N-cadherin, Vimentin and Snail protein levels in CAL27 cells, whilst E2F7 high-expression exhibited the opposite effects in TCA-83 cells. Conclusions These outcomes indicated that E2F7 performs a carcinogenic role in OSCC, which provides a theoretical basis for the therapeutic strategies of OSCC.

Evaluation of the Cytotoxic Activity of Crocin and Safranal, Constituents of Saffron, in Oral Squamous Cell Carcinoma (KB Cell Line)

2017 ◽  
Vol 69 (6) ◽  
pp. 911-919 ◽  
Author(s):  
Raheleh Jabini ◽  
Melika Ehtesham-Gharaee ◽  
Zohreh Dalirsani ◽  
Fatemeh Mosaffa ◽  
Zahra Delavarian ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cytotoxic Activity ◽  
Cell Carcinoma ◽  
Cell Line ◽  
Squamous Cell

scholarly journals Evaluation of Hyaluronic Acid to Modulate Oral Squamous Cell Carcinoma Growth In Vitro

2020 ◽  
Vol 11 (4) ◽  
pp. 72
Author(s):  
Jordan Ringer ◽  
Bryan Morrison ◽  
Karl Kingsley
Keyword(s):  
Growth Rate ◽  
Squamous Cell Carcinoma ◽  
Hyaluronic Acid ◽  
Oral Squamous Cell Carcinoma ◽  
Tumor Growth ◽  
Cell Carcinoma ◽  
Cell Lines ◽  
Squamous Cell ◽  
Chemotherapeutic Agents ◽  
Oral Tumor

Introduction: Previous studies have demonstrated that glycosaminoglycan hyaluronic acid (HA) is capable of mediating oral tumor growth. Some clinical evidence has suggested reduced HA expression predicts poor cancer prognosis and that HA-chemotherapy conjugates may function synergistically to inhibit oral tumor growth. Other studies have found conflicting results that suggest enhanced CD44-HA-mediated growth and proliferation. Due to the lack of clarity regarding HA function, the primary goal of this study was to investigate the effects of HA using well-characterized oral cancer cell lines. Methods: Using several commercially available oral squamous cell carcinoma lines (and a normal non-cancerous control), 96-well growth and viability assays were conducted using HA (alone and in combination with chemotherapeutic agents paclitaxel and PD98059). Results: Different results were observed in each of the cell lines evaluated. HA induced small, non-significant changes in cellular viability among each of the cell lines within a narrow range (1–8%), p = 0.207. However, HA induced differing effects on growth, with minimal, non-significant changes among some cell lines, such as SCC4 (+1.7%), CCL-30 (−2.8%), and SCC15 (−2.5%), p = 0.211 and more robust inhibition among other cell lines, SCC9 (−24.4%), SCC25 (−36.6%), and CAL27 (−47.8%), p = 0.0001. Differing effects were also observed with growth and viability under concomitant administration of HA with PD98059 or paclitaxel. Further analysis of these data revealed strong inverse (Pearson’s) correlations between initial baseline growth rate and responsiveness to HA administration, ranging from R = −0.27 to R = −0.883. Conclusion: The results of this study revealed differing responses to HA, which may be inversely correlated with intrinsic characteristics, such as the baseline growth rate. This may suggest that the more rapidly growing cell lines are more responsive to combination therapy with hyaluronic acid; an important finding that may provide insights into the mechanisms responsible for these observations.

scholarly journals Genetically-defined novel oral squamous cell carcinoma cell lines for the development of molecular therapies

Oncotarget ◽  
2016 ◽  
Vol 7 (19) ◽  
pp. 27802-27818 ◽  
Author(s):  
Muhammad Zaki Hidayatullah Fadlullah ◽  
Ivy Kim-Ni Chiang ◽  
Kalen R. Dionne ◽  
Pei San Yee ◽  
Chai Phei Gan ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Cell Lines ◽  
Squamous Cell ◽  
Carcinoma Cell ◽  
Squamous Cell Carcinoma Cell ◽  
Carcinoma Cell Lines ◽  
Molecular Therapies
Sign in / Sign up

Export Citation Format

Share Document