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 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 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 Costunolide Induces Apoptosis via the Reactive Oxygen Species and Protein Kinase B Pathway in Oral Cancer Cells

2021 ◽  
Vol 22 (14) ◽  
pp. 7509
Author(s):  
Hai Huang ◽  
Jun-Koo Yi ◽  
Su-Geun Lim ◽  
Sijun Park ◽  
Haibo Zhang ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Cycle ◽  
Flow Cytometry ◽  
Oral Cancer ◽  
Cancer Cells ◽  
Reactive Oxygen ◽  
Migration And Invasion ◽  
Oxygen Species ◽  
Oral Cancer Cells

Oral cancer (OC) has been attracted research attention in recent years as result of its high morbidity and mortality. Costunolide (CTD) possesses potential anticancer and bioactive abilities that have been confirmed in several types of cancers. However, its effects on oral cancer remain unclear. This study investigated the potential anticancer ability and underlying mechanisms of CTD in OC in vivo and in vitro. Cell viability and anchorage-independent colony formation assays were performed to examine the antigrowth effects of CTD on OC cells; assessments for migration and invasion of OC cells were conducted by transwell; Cell cycle and apoptosis were investigated by flow cytometry and verified by immunoblotting. The results revealed that CTD suppressed the proliferation, migration and invasion of oral cancer cells effectively and induced cell cycle arrest and apoptosis; regarding the mechanism, CTD bound to AKT directly by binding assay and repressed AKT activities through kinase assay, which thereby downregulating the downstream of AKT. Furthermore, CTD remarkably promotes the generation of reactive oxygen species by flow cytometry assay, leading to cell apoptosis. Notably, CTD strongly suppresses cell-derived xenograft OC tumor growth in an in vivo mouse model. In conclusion, our results suggested that costunolide might prevent progression of OC and promise to be a novel AKT inhibitor.

scholarly journals CSN8 is a key regulator in hypoxia-induced epithelial–mesenchymal transition and dormancy of colorectal cancer cells

2020 ◽  
Vol 19 (1) ◽  
Author(s):  
Songwen Ju ◽  
Feng Wang ◽  
Yirong Wang ◽  
Songguang Ju
Keyword(s):  
Colorectal Cancer ◽  
Cancer Cells ◽  
Cancer Progression ◽  
Epithelial Mesenchymal Transition ◽  
Migration And Invasion ◽  
Mesenchymal Transition ◽  
Treatment Conditions ◽  
Colorectal Cancer Cells

AbstractHypoxic stress plays a pivotal role in cancer progression; however, how hypoxia drives tumors to become more aggressive or metastatic and adaptive to adverse environmental stress is still poorly understood. In this study, we revealed that CSN8 might be a key regulatory switch controlling hypoxia-induced malignant tumor progression. We demonstrated that the expression of CSN8 increased significantly in colorectal cancerous tissues, which was correlated with lymph node metastasis and predicted poor patient survival. CSN8 overexpression induces the epithelial-mesenchymal transition (EMT) process in colorectal cancer cells, increasing migration and invasion. CSN8 overexpression arrested cell proliferation, upregulated key dormancy marker (NR2F1, DEC2, p27) and hypoxia response genes (HIF-1α, GLUT1), and dramatically enhanced survival under hypoxia, serum deprivation, or chemo-drug 5-fluorouracil treatment conditions. In particular, silenced CSN8 blocks the EMT and dormancy processes induced by the hypoxia of 1% O2 in vitro and undermines the adaptive capacity of colorectal cancer cells in vivo. The further study showed that CSN8 regulated EMT and dormancy partly by activating the HIF-1α signaling pathway, which increased HIF-1α mRNA expression by activating NF-κB and stabilized the HIF-1α protein via HIF-1α de-ubiquitination. Taken together, CSN8 endows primary colorectal cancer cells with highly aggressive/metastatic and adaptive capacities through regulating both EMT and dormancy induced by hypoxia. CSN8 could serve as a novel prognostic biomarker for colorectal cancer and would be an ideal target of disseminated dormant cell elimination and tumor metastasis, recurrence, and chemoresistance prevention.

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

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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