scholarly journals Cell-Type-Specific Chromatin States Differentially Prime Squamous Cell Carcinoma Tumor-Initiating Cells for Epithelial to Mesenchymal Transition

2017 ◽  
Vol 20 (2) ◽  
pp. 191-204.e5 ◽  
Author(s):  
Mathilde Latil ◽  
Dany Nassar ◽  
Benjamin Beck ◽  
Soufiane Boumahdi ◽  
Li Wang ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Epithelial To Mesenchymal Transition ◽  
Cell Type ◽  
Tumor Initiating Cells ◽  
Mesenchymal Transition ◽  
Squamous Cell Carcinoma Tumor ◽  
Cell Type Specific ◽  
Carcinoma Tumor

scholarly journals Markers of Epithelial to Mesenchymal Transition in Association with Survival in Head and Neck Squamous Cell Carcinoma (HNSCC)

PLoS ONE ◽  
2014 ◽  
Vol 9 (4) ◽  
pp. e94273 ◽  
Author(s):  
Eirini Pectasides ◽  
Theodoros Rampias ◽  
Clarence Sasaki ◽  
Christos Perisanidis ◽  
Vassilis Kouloulias ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Head And Neck ◽  
Squamous Cell ◽  
Epithelial To Mesenchymal Transition ◽  
Neck Squamous Cell Carcinoma ◽  
Mesenchymal Transition

Effect of a diffractive grid applied to laryngeal images with squamous cell carcinoma tumor

2021 ◽  
Author(s):  
Jacilene Martins Medeiros ◽  
Giuseppe Antônio Cirino ◽  
Arlindo Neto Montagnoli
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Squamous Cell Carcinoma Tumor ◽  
Carcinoma Tumor

scholarly journals Extracellular Vesicle-Mediated Chemoresistance in Oral Squamous Cell Carcinoma

2021 ◽  
Vol 8 ◽  
Author(s):  
Zhu-Jun Law ◽  
Xin Hui Khoo ◽  
Pei Tee Lim ◽  
Bey Hing Goh ◽  
Long Chiau Ming ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Epithelial To Mesenchymal Transition ◽  
Treatment Options ◽  
Extracellular Vesicle ◽  
High Recurrence Rate ◽  
Mesenchymal Transition ◽  
Persistent Problem

Oral Squamous Cell Carcinoma (OSCC) remains a cancer with poor prognosis and high recurrence rate. Even with multimodal treatment options available for OSCC, tumor drug resistance is still a persistent problem, leading to increased tumor invasiveness among OSCC patients. An emerging trend of thought proposes that extracellular vesicles (EVs) play a role in facilitating tumor progression and chemoresistance via signaling between tumor cells. In particular, exosomes and microvesicles are heavily implicated in this process by various studies. Where primary studies into a particular EV-mediated chemoresistance mechanism in OSCC are limited, similar studies on other cancer cell types will be used in the discussion below to provide ideas for a new line of investigation into OSCC chemoresistance. By understanding how EVs are or may be involved in OSCC chemoresistance, novel targeted therapies such as EV inhibition may be an effective alternative to current treatment options in the near future. In this review, the current understandings on OSCC drug mechanisms under the novel context of exosomes and microvesicles were reviewed, including shuttling of miRNA content, drug efflux, alteration of vesicular pH, anti-apoptotic signaling, modulation of DNA damage repair, immunomodulation, epithelial-to-mesenchymal transition and maintenance of tumor by cancer stem cells.

scholarly journals RANK Ligand Modulation of Autophagy in Oral Squamous Cell Carcinoma Tumor Cells

2015 ◽  
Vol 117 (1) ◽  
pp. 118-125 ◽  
Author(s):  
Yuvaraj Sambandam ◽  
Sashank Sakamuri ◽  
Sundaravadivel Balasubramanian ◽  
Azizul Haque
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Tumor Cells ◽  
Squamous Cell ◽  
Rank Ligand ◽  
Squamous Cell Carcinoma Tumor ◽  
Carcinoma Tumor

scholarly journals PADI4 stimulates esophageal squamous cell carcinoma tumor growth and up‐regulates CA9 expression

2018 ◽  
Vol 58 (1) ◽  
pp. 66-75 ◽  
Author(s):  
Chunyan Liu ◽  
Junyi Tang ◽  
Chang Li ◽  
Guangbo Pu ◽  
Dongxia Yang ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Tumor Growth ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Squamous Cell Carcinoma Tumor ◽  
Carcinoma Tumor

(S,R)3-(4-Hydroxyphenyl)-4,5-Dihydro-5-Isoxazole Acetic Acid Methyl Ester Inhibits Epithelial-to-Mesenchymal Transition through TGF-β/Smad4 Axis in Nasopharyngeal Carcinoma

2021 ◽  
Vol 21 ◽  
Author(s):  
Qibing Chen ◽  
Yan Wang ◽  
Fen Li ◽  
Xiang Cheng ◽  
Yu Xiao ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Nasopharyngeal Carcinoma ◽  
Cell Carcinoma ◽  
Head And Neck ◽  
Squamous Cell ◽  
Epithelial To Mesenchymal Transition ◽  
Immunofluorescence Assay ◽  
Migration And Invasion ◽  
Mesenchymal Transition

Background: Macrophage migration inhibitory factor (MIF), originally reported as an inflammation regulating molecule, is elevated in various cancer cells, which may promote carcinogenesis. Meanwhile, ISO-1 is a potent small molecular inhibitor of MIF, which has not been investigated in nasopharyngeal carcinoma (NPC); hence the impact of ISO-1 on NPC cells remains to be illustrated. Objective: This study intended to explore the biological function of ISO-1 in NPC cells in vitro and prove a possibility of ISO-1 being a novel agent in NPC treatments. Methods: Gene expression of MIF in Head and Neck squamous cell carcinoma were obtained from The Cancer Genome Atlas (TCGA) database. Nasal pharyngeal tissues were collected from adult patients undergoing nasopharyngeal biopsy for MIF level detection. Proliferation of NPC cell lines 5-8B and 6-10B was studied using Cell Counting Kit-8 (CCK-8) assay and plate-colony-formation assay, apoptosis was determined by flow cytometry and TUNEL staining, migration and invasion capacities were measured by wound-healing assay and transwell assay, all to explore the function of ISO-1 in NPC cells in vitro. Epithelial-to-mesenchymal transition (EMT) level of NPC cells was determined by Western blot analysis and immunofluorescence assay. Results: Transcript level of MIF was significantly higher in head and neck squamous cell carcinoma. Protein MIF was overexpressed in human NPC tissues compared to non-cancerous ones, and its expression could be compromised by ISO-1 in vitro. 100μM ISO-1 significantly hindered NPC cells migration and invasion capacities in vitro but acted relatively poorly on proliferation and apoptosis. Immunofluorescence assay and Western blotting implied a down-regulated EMT level through TGF-β/Smad4 axis in ISO-1 treated NPC cells compared to the vehicle. Conclusion: This study indicated that MIF antagonist ISO-1 holds impact on NPC progression by influencing the migration and invasion of NPC cells ISO-1 inhibits the EMT process of NPC cells through TGF-β/Smad4 axis, supporting that prudent application of ISO-1 may be a potential adjuvant treatment for NPC.

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