scholarly journals Synthetic Isoliquiritigenin Inhibits Human Tongue Squamous Carcinoma Cells through Its Antioxidant Mechanism

2017 ◽  
Vol 2017 ◽  
pp. 1-11 ◽  
Author(s):  
Cuilan Hou ◽  
Wenguang Li ◽  
Zengyou Li ◽  
Jing Gao ◽  
Zhenjie Chen ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Fluorescence Microscopy ◽  
Gelatin Zymography ◽  
Squamous Carcinoma ◽  
Carcinoma Cells ◽  
Migration And Invasion ◽  
Antioxidant Mechanism ◽  
Squamous Carcinoma Cells ◽  
Human Tongue ◽  
Tongue Squamous Carcinoma

Isoliquiritigenin (ISL), a natural antioxidant, has antitumor activity in different types of cancer cells. However the antitumor effect of ISL on human tongue squamous carcinoma cells (TSCC) is not clear. Here we aimed to investigate the effects of synthetic isoliquiritigenin (S-ISL) on TSCC and elucidate the underlying mechanisms. S-ISL was synthesized and elucidated from its nuclear magnetic resonance spectrum and examined using high performance liquid chromatography. The effects of S-ISL on TSCC cells (Tca8113) were evaluated in relation to cell proliferation, apoptosis and adhesion, migration, and invasion using sulforhodamine B assay, fluorescence microscopy technique, flow cytometry (FCM) analysis, and Boyden chamber assay. The associated regulatory mechanisms were examined using FCM and fluorescence microscopy for intracellular reactive oxygen species (ROS) generation, Gelatin zymography assay for matrix metalloproteinase (MMP) activities, and Western blot for apoptosis regulatory proteins (Bcl-2 and Bax). Our data indicated that S-ISL inhibited Tca8113 cell proliferation, adhesion, migration, and invasion while promoting the cell apoptosis. Such effects were accompanied by downregulation of Bcl-2 and upregulation of Bax, reduction of MMP-2 and MMP-9 activities, and decreased ROS production. We conclude that S-ISL is a promising agent targeting TSCC through multiple anticancer effects, regulated by its antioxidant mechanism.

scholarly journals The Migration and Invasion of Oral Squamous Carcinoma Cells: Matrix, Growth Factor and Signalling Involvement

Cancers ◽  
2021 ◽  
Vol 13 (11) ◽  
pp. 2633
Author(s):  
Ian R. Ellis
Keyword(s):  
Growth Factor ◽  
Cancer Cells ◽  
Squamous Carcinoma ◽  
Carcinoma Cells ◽  
Migration And Invasion ◽  
Squamous Carcinoma Cells ◽  
Oral Squamous Carcinoma

The link between the migration of cancer cells and the spread of cancers has been established for many years [...]

scholarly journals Electrochemical Assessment of Anticancer Compounds on the Human Tongue Squamous Carcinoma Cells

Sensors ◽  
2020 ◽  
Vol 20 (9) ◽  
pp. 2632 ◽  
Author(s):  
Chun-Chung Huang ◽  
Tse-Hua Tung ◽  
Chien-Chu Huang ◽  
Shao-Yi Lin ◽  
Shih-Chi Chao ◽  
...  
Keyword(s):  
Cell Morphology ◽  
Squamous Carcinoma ◽  
Annexin V ◽  
Time Dependent ◽  
Second Primary ◽  
Second Primary Malignancy ◽  
Primary Malignancy ◽  
Squamous Carcinoma Cells ◽  
Human Tongue ◽  
Tongue Squamous Carcinoma

The most common oral cancer is squamous cell carcinoma (SCC) and its highest occurrence is in the tongue. Almost 30% of patients with one primary head and neck tumor will have a second primary malignancy. In recent studies, two novel plant extracts, andrographolide and cannabidiol (CBD), have been exploited for their anticancer effects. Here, we investigated the cytotoxic effects of these two compounds on SCC-25 cells, a human tongue squamous carcinoma cell line, and compared the outcomes with two chemotherapeutic drugs, cisplatin and fluorouracil. Electric cell substrate impedance sensing (ECIS) system was applied to measure frequency- and time-dependent impedance of SCC-25 cell-covered electrodes and to further assess subtle changes in cell morphology and micromotion in response to different concentrations (0, 10, 30, 100, and 300 µM) of these compounds. AlamarBlue and Annexin V/7-AAD binding assays were used to measure the concentration dependent changes in viability and apoptosis of SCC-25 cells. Our results demonstrate that 24 hours after exposure to 30 µM CBD can significantly decrease the micromotion rate, damage the integrity of cell morphology, reduce cell viability, and induce higher apoptosis in treated SCC-25 cells, while the other three drugs attain similar effects at the concentration of 100 µM or higher. The apoptosis-induced changes in cell morphology and micromotion monitored by ECIS correlate well with biochemical assays. Thus, both frequency- and time-dependent impedance measurements using ECIS can be used to real-time follow cancer cell activities in response to anticancer drugs with different temporal cytotoxicity profiles.

Scutellariae radixInduces Apoptosis in Chemoresistant SCC-25 Human Tongue Squamous Carcinoma Cells

2015 ◽  
Vol 43 (01) ◽  
pp. 167-181 ◽  
Author(s):  
Byul-Bora Choi ◽  
Jeong Hae Choi ◽  
Sang-Rye Park ◽  
Ji-Young Kim ◽  
Jin-Woo Hong ◽  
...  
Keyword(s):  
Cell Growth ◽  
Cell Morphology ◽  
Squamous Carcinoma ◽  
Carcinoma Cells ◽  
Mitogen Activated Protein Kinase ◽  
Dependent Manner ◽  
Scutellariae Radix ◽  
Squamous Carcinoma Cells ◽  
Human Tongue ◽  
Oral Squamous Carcinoma

Scutellariae radix is one of the most widely used anticancer herbal medicines in several Asian countries, including Korea, Japan, and China. Squamous cell carcinoma (SCC) is one of the most common head and neck carcinomas, which is highly invasive and metastatic, and can potentially develop chemoresistance. Therefore, new effective treatment methods are urgently needed. We determined the effects of Scutellariae radix on SCC-25 cells using the WST-1 assay, F-actin staining, flow cytometry analysis, immunofluorescence staining, and western blot analysis. Scutellariae radix treatment inhibited SCC-25 cell growth in a dose- and time-dependent manner, but it did not inhibit HaCaT (human keratinocyte) cell growth. Changes in cell morphology and disruption of filamentous (F)-actin organization were observed. Scutellariae radix-induced apoptosis as indicated by the translocation of cytochrome c and apoptosis-inducing factor (AIF) into the nucleus and cytosol. Scutellariae radix-induced an increase in cells with sub-G1 DNA content, and increased Bax, cleaved caspase-3, caspase-7, caspase-9, DNA fragmentation factor 45 (DFF 45), and poly(ADP-ribose) polymerase-1 (PARP-1) expression levels. Furthermore, increased expression of phosphorylated mitogen-activated protein kinase (MAPK)-related proteins was detected. The antitumor effect of Scutellariae radix was due to decreased cell proliferation, changes in cell morphology, and the activation of caspase and MAPK pathways. Taken together, the findings of this study highlight the anticancer activity of Scutellariae radix in chemoresistant SCC-25 oral squamous carcinoma cells.

scholarly journals LncRNA WT1-AS up-regulates p53 to inhibit the proliferation of cervical squamous carcinoma cells

BMC Cancer ◽  
2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Yunxia Zhang ◽  
Renhua Na ◽  
Xinling Wang
Keyword(s):  
Cell Proliferation ◽  
Squamous Carcinoma ◽  
Cervical Squamous Cell Carcinoma ◽  
Hpv Infection ◽  
Carcinoma Cells ◽  
Over Expression ◽  
Squamous Carcinoma Cells ◽  
Measurement Cell ◽  
Cancer Tissues ◽  
Medical University

Abstract Background It has been reported that the development of cervical squamous cell carcinoma (CSCC) requires the involvement of a large number of lncRNAs. In a recent study lncRNA, WT1-AS was been characterized as a tumor-suppressive lncRNA in gastric cancer. In our study we aim to explore the involvement of WT1-AS in CSCC. Methods Seventy-six CSCC patients (20 to 63 years, 40.1 ± 6.1 year) from the 233 CSCC patients who were admitted by the Affiliated Tumour Hospital of Xinjiang Medical University between august 2010 and January 2014. RT-qPCR, cell proliferation rate measurement, cell transfection, and western blot were carried out to analyze the samples. Results We found that HPV infection failed to affect WT1-AS expression in CSCC tissues, while WT1-AS was down-regulated in CSCC tissues compared with non-cancer tissues. P53 was also down-regulated in CSCC tissues and positively correlated with WT1-AS. Analysis of the survival of CSCC patients revealed that low levels of WT1-AS were accompanied by poor survival. Significantly up-regulated p53 was observed after WT1-AS over-expression in CSCC cells, while p53 over-expression failed to affect WT1-AS. P53 and WT1-AS over-expression resulted in the inhibited proliferation of CSCC cells. Conclusion Therefore, WT1-AS is down-regulated in CSCC and it may inhibit CSCC cell proliferation at least partially by up-regulating p53.

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