scholarly journals Antioral Squamous Cell Carcinoma Effects of Carvacrol via Inhibiting Inflammation, Proliferation, and Migration Related to Nrf2/Keap1 Pathway

2021 ◽  
Vol 2021 ◽  
pp. 1-14
Author(s):  
Hui Liu ◽  
Xiaoliang Xu ◽  
Ran Wu ◽  
Lei Bi ◽  
Chunguang Zhang ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Molecular Mechanisms ◽  
Epithelial Mesenchymal Transition ◽  
Mesenchymal Transition ◽  
And Migration ◽  
Related Proteins ◽  
Proliferation And Migration ◽  
E Cadherin

Objective. To observe the therapeutic effect of Carvacrol on oral squamous cell carcinoma (OSCC) and dissect underlying molecular mechanisms. Methods. Keap1/Nrf2, NALP3, Vimentin, and E-cadherin expression was detected in OSCC and normal oral mucosa (NOM) tissues using immunofluorescence or western blot. When treated with Carvacrol or tert-butylhydroquinone (TBHQ) that activates Nrf2, the expression of Keap1/Nrf2/HO-1, epithelial-mesenchymal transition- (EMT-) related proteins, and NALP3 was examined in OSCC cells. Nrf2 was silenced by treatment with sh-Nrf2 or ML385. After silencing Nrf2 or Carvacrol treatment, cell proliferation and migration were assessed by clone formation and scratch and transwell tests in OSCC cells. Moreover, the expression of Keap1/Nrf2/HO-1, EMT-related proteins, and NALP3 was detected. Results. Keap1/Nrf2, NALP3, Vimentin, and E-cadherin proteins were all significantly upregulated in OSCC than NOM tissues. Carvacrol significantly suppressed Keap1/Nrf2/HO-1 activation. Carvacrol or silencing Nrf2 markedly inhibited the expression of Keap1/Nrf2/HO-1, EMT-related proteins, and NALP3 inflammasome in OSCC cells. Furthermore, clone formation and migration capacities were suppressed following treatment with Carvacrol or Nrf2 depletion. The opposite results were found when there is overexpression of Nrf2. However, Carvacrol distinctly improved the cancer-promoting effect induced by Nrf2 overexpression. Conclusion. Our findings suggested that Carvacrol ameliorated inflammation, proliferation, and migration for OSCC, which was related to inhibition of the Nrf2/Keap1 pathway.

scholarly journals Sulfiredoxin may promote metastasis and invasion of cervical squamous cell carcinoma by epithelial–mesenchymal transition

Tumor Biology ◽  
2017 ◽  
Vol 39 (3) ◽  
pp. 101042831769594
Author(s):  
Xiaoyan Chen ◽  
Kangyun Lan ◽  
Qin Liu ◽  
Xue Yang ◽  
Hui Wang
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Epithelial Mesenchymal Transition ◽  
Cervical Squamous Cell Carcinoma ◽  
Expression Level ◽  
Migration Activity ◽  
Mesenchymal Transition ◽  
Siha Cells ◽  
E Cadherin

Sulfiredoxin (Srx), a novel oxidative stress-induced antioxidant protein, has been reported to be expressed in several human tumour tissues. However, the expression and functions of Srx in cervical squamous cell carcinoma remain unknown. Here, we proved that expression of Srx was upregulated in cervical tissues as revealed by immunohistochemistry, and revealed a close correlation between the protein’s expression and the expression level of one core epithelial–mesenchymal transition marker, E-cadherin. We demonstrated that Srx was overexpressed in cervical squamous cell carcinoma and its expression level was closely correlated with lymph node metastasis and invasion of cervical squamous cell carcinoma. Meanwhile, Srx expression was negatively correlated with E-cadherin expression. The remission time (tumour-free status after surgery) of the Srx strong staining group was significantly shorter than that of the Srx weak staining group. We silenced Srx by short hairpin RNA in HeLa and SiHa cells. Diminished Srx expression upregulated E-cadherin expression. The cell invasion and migration activity in the ShSrx group were obviously decreased in HeLa and SiHa cells. Moreover, Srx regulated the expression of the other marker of epithelial–mesenchymal transition, vimentin. In conclusion, the study suggested that Srx was highly expressed in cervical squamous cell carcinoma and may promote invasion and metastasis of cervical squamous cell carcinoma via regulating epithelial–mesenchymal transition.

scholarly journals Epithelial-Mesenchymal Transition in Oral Squamous Cell Carcinoma

ISRN Oncology ◽  
2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Suttichai Krisanaprakornkit ◽  
Anak Iamaroon
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Signaling Pathways ◽  
Squamous Cell ◽  
Molecular Mechanisms ◽  
Epithelial Mesenchymal Transition ◽  
Large Body ◽  
Invasion And Metastasis ◽  
Mesenchymal Transition

Oral cancer is one of the drastic human cancers due to its aggressiveness and high mortality rate. Of all oral cancers, squamous cell carcinoma is the most common accounting for more than 90%. Epithelial-mesenchymal transition (EMT) is suggested to play an important role during cancer invasion and metastasis. Recently, emerging knowledge on EMT in carcinogenesis is explosive, tempting us to analyze previous studies on EMT in oral squamous cell carcinoma (OSCC). In this paper, we have first addressed the general molecular mechanisms of EMT, evidenced by alterations of cell morphology during EMT, the presence of cadherin switching, turning on and turning off of many specific genes, the activation of various signaling pathways, and so on. The remaining part of this paper will focus on recent findings of the investigations of EMT on OSCC. These include the evidence of EMT taking place in OSCC and the signaling pathways employed by OSCC cells during their invasion and metastasis. Collectively, with the large body of new knowledge on EMT in OSCC elaborated here, we are hopeful that targeting treatment for OSCC will be developed.

HPV18 Associated with E-cadherin Expression in Head and Neck Squamous Cell Carcinoma

2018 ◽  
Vol 69 (10) ◽  
pp. 2638-2641 ◽  
Author(s):  
Simina Boia ◽  
Eugen Radu Boia ◽  
Raluca Amalia Ceausu ◽  
Constantin Nicolae Balica ◽  
Ovidiu Alexandru Mederle
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Head And Neck ◽  
Squamous Cell ◽  
Epithelial Mesenchymal Transition ◽  
Neck Squamous Cell Carcinoma ◽  
Mesenchymal Transition ◽  
Poorly Differentiated ◽  
Well Differentiated ◽  
E Cadherin

HPV is an important oropharyngeal cancer cause, but it may have a role in other head and neck cancers? HPVpositive head and neck squamous cell carcinoma (HNSCC) epithelial-mesenchymal transition role is unclear. We included 38 cases: 20 laryngeal, 3 corresponding lymph nodes; 5 oropharyngeal, 5 hypopharyngeal, 2 rhynopahryngeal, 2 pharyngolaryngeal and 1 naso-sinusal case. Immunoreactivity was positive in nuclear expression cells, accordingly: score 1 (10-30%), 2 (30-50%) and 3 (]50%). HPV18 immunoexpression appeared in 18 cases (47.36%), (11 laryngeal, 4 oropharyngeal, 1 hypopharyngeal, 1 pharyngolaryngeal and 1 naso-sinusal). The score was 1 in larynx well differentiated type. The score was between 1 and 3 in larynx moderately differentiated types, and a significant correlation HPV18/E-cadherin was found (p=0.031). HPV18+/E-cadherin low values were noticed in larynx, oropharynx, pharyngo-larynx and naso-sinusal well and moderately differentiated types. HPV18-/E-cadherin low values were present in larynx, hypo and rhyno-pharynx moderately and poorly differentiated and larynx well differentiated types. Larynx presented HPV18/E-cadherin and moderately differentiated type significant correlation. Rhyno, hypo-pharyngeal and laryngeal presented HPV18�/E-cadherin low values association for moderately, poorly and undifferentiated types. The oropharyngeal location was associated with E-cadherin maximum values, independently of HPV18 status.

The prognostic role of the epithelial-mesenchymal transition markers E-cadherin and Slug in laryngeal squamous cell carcinoma

2015 ◽  
Vol 67 (4) ◽  
pp. 491-500 ◽  
Author(s):  
Rocco Cappellesso ◽  
Gino Marioni ◽  
Marika Crescenzi ◽  
Luciano Giacomelli ◽  
Vincenza Guzzardo ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Laryngeal Squamous Cell Carcinoma ◽  
Epithelial Mesenchymal Transition ◽  
Prognostic Role ◽  
Mesenchymal Transition ◽  
E Cadherin

LGR5 promotes invasion and migration by regulating YAP activity in hypopharyngeal squamous cell carcinoma cells

2020 ◽  
Author(s):  
Zijia Zhu ◽  
Shuyuan Yu ◽  
Jihong Wen ◽  
Ping Wang
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Epithelial Mesenchymal Transition ◽  
Tumor Proliferation ◽  
Mesenchymal Transition ◽  
Hypopharyngeal Squamous Cell Carcinoma ◽  
Inflammatory Microenvironment ◽  
Lgr5 Expression ◽  
Related Proteins

Abstract Background High leucine-rich repeat-containing G-protein coupled receptor 5 (LGR5) expression caused by an inflammatory microenvironment was reported to promote tumor proliferation and the epithelial–mesenchymal transition (EMT) in various malignant tumors, but those effects have not been studied in hypopharyngeal squamous cell carcinoma (HSCC) and the molecular mechanism remains unclear. Additionally, YAP/TAZ, an upstream or downstream factor of multiple signaling pathways, can promote tumor proliferation, invasion, and angiogenesis. Our study was aimed to determine whether YAP/TAZ is involved in the regulation of LGR5 expression in the inflammatory microenvironment.Methods We stimulated FaDu cells, a hypopharyngeal squamous cell carcinoma cell line, with inflammatory medium. The expression levels of EMT-related proteins, LGR5, and p-YAP were detected by reverse transcription–polymerase chain reaction, western blotting, and immunofluorescence.Results The results showed that LGR5 expression and the EMT process were significantly enhanced. The expression of EMT-related proteins was up-regulated, while that of p-YAP was decreased. After inhibiting the high LGR5 expression with short interfering RNA, the expression of EMT-related proteins was also down-regulated, while that of p-YAP was significantly increased. The use of verteporfin (VP), an inhibitor of YAP activity that promotes YAP phosphorylation, did not affect LGR5 expression.Conclusions Our findings suggest that the inflammatory microenvironment leads to high LGR5 expression, up-regulating the expression of EMT-related proteins by inhibiting the YAP phosphorylation.

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