Pomegranate extract inhibits migration and invasion of oral cancer cells by downregulating matrix metalloproteinase‐2/9 and epithelial‐mesenchymal transition

2020 ◽  
Vol 35 (6) ◽  
pp. 673-682 ◽  
Author(s):  
Sheng‐Yao Peng ◽  
Chien‐Chou Hsiao ◽  
Ting‐Hsun Lan ◽  
Ching‐Yui Yen ◽  
Ammad A. Farooqi ◽  
...  
Keyword(s):  
Oral Cancer ◽  
Matrix Metalloproteinase ◽  
Cancer Cells ◽  
Epithelial Mesenchymal Transition ◽  
Matrix Metalloproteinase 2 ◽  
Migration And Invasion ◽  
Mesenchymal Transition ◽  
Oral Cancer Cells

scholarly journals PlatyphyllenoneExerts Anti-Metastatic Effects on Human Oral Cancer Cells by Modulating Cathepsin L Expression, MAPK Pathway and Epithelial–Mesenchymal Transition

2021 ◽  
Vol 22 (9) ◽  
pp. 5012
Author(s):  
V. Bharath Kumar ◽  
Jen-Tsun Lin ◽  
B. Mahalakshmi ◽  
Yi-Ching Chuang ◽  
Hsin-Yu Ho ◽  
...  
Keyword(s):  
Oral Cancer ◽  
Cancer Cells ◽  
Epithelial Mesenchymal Transition ◽  
Mapk Pathway ◽  
Cathepsin L ◽  
Mapk Signaling ◽  
Cancer Prognosis ◽  
Migration And Invasion ◽  
Mesenchymal Transition ◽  
Oral Cancer Cells

Advanced-stage oral cancers with lymph node metastasis are associated with poor prognosis and a high mortality rate. Although recent advancement in cancer treatment has effectively improved the oral cancer prognosis, the majority of therapeutic interventions are highly expensive and are associated with severe sideeffects. In the present study, we studied the efficacy of a diarylheptanoid derivative, platyphyllenone, in modulating the metastatic potential of human oral cancer cells. Specifically, we treated the human oral cancer cells (FaDu, Ca9-22, and HSC3) with different concentrations of platyphyllenone and measured the cell proliferation, migration, and invasion. The study findings revealed that platyphyllenonesignificantly inhibited the motility, migration, and invasion of human oral cancer cells. Mechanistically, platyphyllenone reduced p38 phosphorylation, decreased β-catenin and Slug, increased E-cadherin expression, and reduced cathepsin L expression, which collectively led to a reduction in cancer cell migration and invasion. Taken together, our study indicates that platyphyllenone exerts significant anti-metastatic effects on oral cancer cells by modulating cathepsin L expression, the MAPK signaling pathway, and the epithelial–mesenchymal transition process.

scholarly journals Gallic acid inhibits migration and invasion of SCC-4 human oral cancer cells through actions of NF-κB, Ras and matrix metalloproteinase-2 and -9

2014 ◽  
Vol 32 (1) ◽  
pp. 355-361 ◽  
Author(s):  
CHAO-LIN KUO ◽  
KUANG-CHI LAI ◽  
YI-SHIH MA ◽  
SHU-WEN WENG ◽  
JING-PIN LIN ◽  
...  
Keyword(s):  
Oral Cancer ◽  
Matrix Metalloproteinase ◽  
Cancer Cells ◽  
Gallic Acid ◽  
Matrix Metalloproteinase 2 ◽  
Migration And Invasion ◽  
Oral Cancer Cells

scholarly journals Carbonic Anhydrase III Promotes Cell Migration and Epithelial–Mesenchymal Transition in Oral Squamous Cell Carcinoma

Cells ◽  
2020 ◽  
Vol 9 (3) ◽  
pp. 704 ◽  
Author(s):  
Yin-Hung Chu ◽  
Chun-Wen Su ◽  
Yih-Shou Hsieh ◽  
Pei-Ni Chen ◽  
Chiao-Wen Lin ◽  
...  
Keyword(s):  
Cell Migration ◽  
Oral Cancer ◽  
Carbonic Anhydrase ◽  
Cancer Cells ◽  
Epithelial Mesenchymal Transition ◽  
Migration And Invasion ◽  
Mesenchymal Transition ◽  
Src Signaling ◽  
Carbonic Anhydrase Iii ◽  
Oral Cancer Cells

Epithelial–mesenchymal transition (EMT) is strongly correlated with tumor metastasis and contains several protein markers, such as E-cadherin. Carbonic anhydrase III (CA III) exhibits low carbon dioxide hydratase activity in cancer. However, the detailed mechanisms of CA III and their roles in oral cancer are still unknown. This study established a CA III-overexpressed stable clone and observed the expression of CA III protein in human SCC-9 and SAS oral cancer cell lines. The migration and invasion abilities were determined using a Boyden chamber assay. Our results showed that the overexpression of CA III protein significantly increased the migration and invasion abilities in oral cancer cells. Moreover, a whole genome array analysis revealed that CA III regulated epithelial–mesenchymal transition by reducing the expression of epithelial markers. Data from the GEO database also demonstrated that CA III mRNA is negatively correlated with CDH1 mRNA. Mechanistically, CA III increased the cell motility of oral cancer cells through the FAK/Src signaling pathway. In conclusion, this suggests that CA III promotes EMT and cell migration and is potentially related to the FAK/Src signaling pathway in oral cancer.

scholarly journals Melatonin Inhibits Reactive Oxygen Species-Driven Proliferation, Epithelial-Mesenchymal Transition, and Vasculogenic Mimicry in Oral Cancer

2018 ◽  
Vol 2018 ◽  
pp. 1-13 ◽  
Author(s):  
Rui Liu ◽  
Hui-li Wang ◽  
Man-jing Deng ◽  
Xiu-jie Wen ◽  
Yuan-yuan Mo ◽  
...  
Keyword(s):  
Oral Cancer ◽  
Cancer Cells ◽  
Epithelial Mesenchymal Transition ◽  
Vasculogenic Mimicry ◽  
Akt Signaling ◽  
Migration And Invasion ◽  
Apoptosis Resistance ◽  
Mesenchymal Transition ◽  
Oral Cancer Cells

Globally, oral cancer is the most common type of head and neck cancers. Melatonin elicits inhibitory effects on oral cancer; however, the biological function of melatonin and underlying mechanisms remain largely unknown. In this study, we found that melatonin impaired the proliferation and apoptosis resistance of oral cancer cells by inactivating ROS-dependent Akt signaling, involving in downregulation of cyclin D1, PCNA, and Bcl-2 and upregulation of Bax. Melatonin inhibited the migration and invasion of oral cancer cells by repressing ROS-activated Akt signaling, implicating with the reduction of Snail and Vimentin and the enhancement of E-cadherin. Moreover, melatonin hampered vasculogenic mimicry of oral cancer cells through blockage of ROS-activated extracellular-regulated protein kinases (ERKs) and Akt pathways involving the hypoxia-inducible factor 1α. Consistently, melatonin retarded tumorigenesis of oral cancerin vivo. Overall, these findings indicated that melatonin exerts antisurvival, antimotility, and antiangiogenesis effects on oral cancer partly by suppressing ROS-reliant Akt or ERK signaling.

scholarly journals DOC1-Dependent Recruitment of NURD Reveals Antagonism with SWI/SNF during Epithelial-Mesenchymal Transition in Oral Cancer Cells

Cell Reports ◽  
2017 ◽  
Vol 20 (1) ◽  
pp. 61-75 ◽  
Author(s):  
Adone Mohd-Sarip ◽  
Miriam Teeuwssen ◽  
Alice G. Bot ◽  
Maria J. De Herdt ◽  
Stefan M. Willems ◽  
...  
Keyword(s):  
Oral Cancer ◽  
Cancer Cells ◽  
Epithelial Mesenchymal Transition ◽  
Mesenchymal Transition ◽  
Oral Cancer Cells

Gypenosides inhibits migration and invasion of human oral cancer SAS cells through the inhibition of matrix metalloproteinase-2 -9 and urokinase-plasminogen by ERK1/2 and NF-kappa B signaling pathways

2010 ◽  
Vol 30 (5) ◽  
pp. 406-415 ◽  
Author(s):  
Kung-Wen Lu ◽  
Jung-Chou Chen ◽  
Tung-Yuan Lai ◽  
Jai-Sing Yang ◽  
Shu-Wen Weng ◽  
...  
Keyword(s):  
Oral Cancer ◽  
Matrix Metalloproteinase ◽  
Cancer Cells ◽  
Time Dependent ◽  
Migration And Invasion ◽  
Mrna Levels ◽  
Dependent Manner ◽  
Invasion And Migration ◽  
Oral Cancer Cells ◽  
And Migration

Gypenosides (Gyp), found in Gynostemma pentaphyllum Makino, has been used as a folk medicine in the Chinese population for centuries and is known to have diverse pharmacologic effects, including anti-proliferative and anti-cancer actions. However, the effects of Gyp on prevention from invasion and migration of oral cancer cells are still unsatisfactory. The purpose of this study was to investigate effects of Gyp treatment on migration and invasion of SAS human oral cancer cells. SAS cells were cultured in the presence of 90 and 180 μg/mL Gyp for 24 and 48 hours. Gyp induced cytotoxic effects and inhibited SAS cells migration and invasion in dose- and time-dependent response. Wound-healing assay and boyden chamber assay were carried out to investigate Gyp-inhibited migration and invasion of SAS cells. Gyp decreased the abundance of several proteins, including nuclear factor-kappa B (NF-κB), cyclooxygenase-2 (COX-2), extracellular signal-regulated kinase 1/2 (ERK1/ 2), matrix metalloproteinase-9, -2 (MMP-9, -2), sevenless homolog (SOS), Ras, urokinase-type plasminogen activator (uPA), focal adhesion kinase (FAK) and RAC-alpha serine/threonine-protein kinase (Akt), in a time-dependent manner. In addition, Gyp decreased mRNA levels of MMP-2, MMP-7, MMP-9 but did not affect FAK and Rho A mRNA levels in SAS cells. These results provide evidences for the role of Gyp as a potent anti-metastatic agent, which can markedly inhibit the metastatic and invasive capacity of oral cancer cells. The inhibition of NF-κB and MMP-2, -7 and -9 signaling may be one of the mechanisms that is present in Gyp-inhibited cancer cell invasion and migration.

P3.31. Role of GSK-3β as a negative regulator of epithelial-mesenchymal transition in oral cancer cells

2009 ◽  
Vol 3 (1) ◽  
pp. 210-211
Author(s):  
J.H. Kang ◽  
J.J. Joung ◽  
J.B. Cho ◽  
P.Y. Yun ◽  
J.H. Lee ◽  
...  
Keyword(s):  
Oral Cancer ◽  
Cancer Cells ◽  
Epithelial Mesenchymal Transition ◽  
Negative Regulator ◽  
Mesenchymal Transition ◽  
Oral Cancer Cells ◽  
Gsk 3Β

scholarly journals Curcumin inhibits epithelial‑mesenchymal transition in oral cancer cells via c‑Met blockade

2020 ◽  
Author(s):  
Yuichi Ohnishi ◽  
Tsukasa Sakamoto ◽  
Li Zhengguang ◽  
Hiroki Yasui ◽  
Hiroyuki Hamada ◽  
...  
Keyword(s):  
Oral Cancer ◽  
Cancer Cells ◽  
Epithelial Mesenchymal Transition ◽  
Mesenchymal Transition ◽  
Oral Cancer Cells

scholarly journals MicroRNA-133 Targets Phosphodiesterase 1C in Drosophila and Human Oral Cancer Cells to Regulate Epithelial-Mesenchymal Transition

2021 ◽  
Vol 12 (17) ◽  
pp. 5296-5309
Author(s):  
Ji Eun Jung ◽  
Joo Young Lee ◽  
Hae Ryoun Park ◽  
Ji Wan Kang ◽  
Yun Hak Kim ◽  
...  
Keyword(s):  
Oral Cancer ◽  
Cancer Cells ◽  
Epithelial Mesenchymal Transition ◽  
Mesenchymal Transition ◽  
Oral Cancer Cells
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