scholarly journals Significant Role of Collagen XVII And Integrin β4 in Migration and Invasion of The Less Aggressive Squamous Cell Carcinoma Cells

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Jyri M. Moilanen ◽  
Stefanie Löffek ◽  
Nina Kokkonen ◽  
Sirpa Salo ◽  
Juha P. Väyrynen ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Significant Role ◽  
Squamous Cell ◽  
Carcinoma Cells ◽  
Migration And Invasion ◽  
Collagen Xvii ◽  
Integrin Β4

HPV 16 E6 Promotes Growth and Metastasis of Esophageal Squamous Cell Carcinoma cells in vitro

2021 ◽  
Author(s):  
Jiao Jiao Hu ◽  
Yu Ji ◽  
Ting Ting Miao ◽  
Shi Yao Zheng ◽  
Xiao Bin Cui ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Mrna Level ◽  
Hpv Infection ◽  
Carcinoma Cells ◽  
Migration And Invasion ◽  
Hpv16 E6

Abstract BackgroundEsophageal squamous cell carcinoma (ESCC) is one of the most lethal malignancies. Increasing evidence has revealed that Human Papillomavirus (HPV) infection may be associated with the possible etiology of ESCC. Nevertheless, the precise role of HPV in ESCC remains unclear.MethodsProliferation and apoptosis capability of ESCC cells upon infection of HPV16 E6 were detected by CCK-8 assay and Western blotting analysis. Wound healing assay and Transwell experiment were conducted to determine the ability of migration and invasion, and the mRNA expression of E6AP, p53, miR-34a was determined by real-time PCR after transfected with HPV16 E6 plasmid. ResultsIn ESCC cells, the ability of proliferation, migration and invasion were increased, and the ability of apoptosis was decreased after transfected with HPV16 E6 plasmid. Furthermore, the mRNA level of E6AP, P53 and miR-34a were decreased in HPV16 E6-transfected cell lines.ConclusionsOur results not only provide evidence that in ESCC, HPV16 E6 promotes cell proliferation, migration and invasion, inhibits cell apoptosis, but also suggest that there may be a correlation between E6AP, P53 and miR-34a in HPV-transfected cell lines. These findings indicated that HPV16 E6 may play an important role in the development of ESCC.

scholarly journals Huaier Inhibits Proliferation, Migration, and Invasion of Cutaneous Squamous Cell Carcinoma Cells by Inhibiting the Methylation Levels of CDKN2A and TP53

2021 ◽  
Vol 20 ◽  
pp. 153473542110316
Author(s):  
Liang Wang ◽  
Lei Xu ◽  
Yu Wang
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Dna Methyltransferase ◽  
Cutaneous Squamous Cell Carcinoma ◽  
Migration And Invasion ◽  
Dependent Manner ◽  
Concentration Gradients ◽  
A431 Cells

Cutaneous squamous cell carcinoma (CSCC) is a malignant tumor that originates from keratinocytes in the epidermis or appendage. Traditional Chinese medicine Huaier has anti-tumor activity in various malignancies. Little is known about the role of Huaier in CSCC. Here, we investigated the function of Huaier in CSCC. We treated CSCC cell line (SCL-1 and A431) with a series of concentration gradients of Huaier to examine the half maximal inhibitory concentration (IC50) of Huaier on SCL-1 and A431 cells. The IC50 of Huaier on growth of SCL-1 and A431 cells were 6.96 and 7.57 mg/mL, respectively. Moreover, Huaier reduced the methylation levels of CDKN2A and TP53, and enhanced the expression of CDKN2A and TP53 in SCL-1 and A431 cells in a dosage-dependent manner. The expression of DNA methyltransferase DNMT1 was severely repressed by Huaier treatment in SCL-1 and A431 cells. DNMT1 overexpression enhanced the methylation levels of CDKN2A and TP53, and suppressed the expression of CDKN2A and TP53 in Huaier-treated SCL-1 and A431 cells. Huaier treatment inhibited proliferation, migration, and invasion of SCL-1 and A431 cells. However, inhibition of CDKN2A or TP53 reversed the influence of Huaier treatment on proliferation, migration, and invasion of CSCC cells. In conclusion, our data demonstrate that Huaier inhibits proliferation, migration, and invasion of CSCC cells by regulating DNA methylation of CDKN2A and TP53, thereby attenuating the progression of CSCC. Thus, Huaier extract may act as a drug for treating CSCC.

scholarly journals Partition-Defective 3 (PARD3) Regulates Proliferation, Apoptosis, Migration, and Invasion in Esophageal Squamous Cell Carcinoma Cells

2017 ◽  
Vol 23 ◽  
pp. 2382-2390 ◽  
Author(s):  
Lei Wang ◽  
Haiping Zhang ◽  
Ayshamgul Hasim ◽  
Abuduaini Tuerhong ◽  
Zhichao Hou ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Carcinoma Cells ◽  
Migration And Invasion

scholarly journals HOXB7 acts as an oncogenic biomarker in head and neck squamous cell carcinoma

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Xiang Wu ◽  
Jin Li ◽  
Tingyuan Yan ◽  
Xueping Ke ◽  
Xin Li ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Head And Neck ◽  
Expression Pattern ◽  
Squamous Cell ◽  
Neck Squamous Cell Carcinoma ◽  
Clinicopathological Parameters ◽  
Migration And Invasion ◽  
Connectivity Map

Abstract Background The homeobox gene Homeobox B7 (HOXB7) is overexpressed across a range of cancers and promotes tumorigenesis through varying effects on proliferation, survival, migration and invasion. However, its expression pattern and oncogenic role of HOXB7 in head and neck squamous cell carcinoma (HNSCC) remain largely unexplored. Here, we aimed to explore the expression pattern of HOXB7, its clinical significance as well as functional roles in HNSCC. Methods HOXB7 mRNA expression in HNSCC was determined by data mining and analyses from TCGA (The Cancer Genome Atlas) and GEO (Gene Expression Omnibus) datasets. The protein abundance of HOXB7 was measured by immunohistochemistry in 119 primary HNSCC samples and associations between its expression and clinicopathological parameters and patient survival were evaluated. The pro-tumorigenic roles of HOXB7 in HNSCC were further delineated in vitro by loss-of-function assay. And a xenograft tumor model was established in nude mice to assess the role of HOXB7 in tumor growth. Connectivity Map (CMap) analysis was performed to identify bioactive small molecules which might be potential inhibitors for HOXB7. Results Bioinformatics analyses showed that HOXB7 mRNA was significantly overexpressed in 8 independent HNSCC datasets from TCGA and GEO databases. HOXB7 protein was markedly upregulated in HNSCC samples as compared to normal counterparts and its overexpression significantly associated with high pathological grade, advanced clinical stage, cervical node metastasis (P = 0.0195, 0.0152, 0.0300) and reduced overall and disease-free survival (P = 0.0014, 0.0007). Univariate and multivariate Cox regression analyses further revealed HOXB7 as an independent prognostic factor for patients’ overall survival. Moreover, HOXB7 knockdown significantly inhibited cell proliferation, migration and invasion and induced cell apoptosis in HNSCC cells, and resulted in compromised tumour growth in vivo. Furthermore, CMap (Connectivity map) analysis has identified three potential bioactive small molecule inhibitors (NU-1025, thiamine, vinburnine) for HOXB7 targeted therapy in HNSCC. Conclusions Our findings revealed that overexpression of HOXB7 was associates with tumour aggressiveness and unfavourable prognosis by serving a novel prognostic biomarker in HNSCC. Moreover, HOXB7 might be involved in the development and progression of HNSCC as an oncogene, and thereby might be a potential therapeutic target for HNSCC.

PS02.201: EXPRESSION AND ROLE OF CLIC1 IN HUMAN ESOPHAGEAL SQUAMOUS CELL CARCINOMA

2018 ◽  
Vol 31 (Supplement_1) ◽  
pp. 179-179
Author(s):  
Toshiyuki Kobayashi ◽  
Atsushi Shiozaki ◽  
Hitoshi Fujiwara ◽  
Hirotaka Konishi ◽  
Yoshito Nako ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Microarray Analysis ◽  
Squamous Cell ◽  
Migration And Invasion ◽  
Poor Prognostic Factor ◽  
Weak Expression

Abstract Background Recent studies have reported important roles for chloride intracellular channel 1 (CLIC1) in various cancers; however, its involvement in esophageal squamous cell carcinoma (ESCC) remains unclear. The aim of the present study was to investigate the role of CLIC1 in human ESCC. Methods CLIC1 expression in human ESCC cell lines was analyzed by Western blotting. Knockdown experiments were conducted with CLIC1 siRNA, and their effects on cell proliferation, the cell cycle, apoptosis, migration, and invasion were analyzed. The gene expression profiles of cells were analyzed using a microarray analysis. An immunohistochemical analysis was performed on 61 primary tumor samples obtained from ESCC patients who underwent esophagectomy. Results ESCC cells strongly expressed CLIC1. The depletion of CLIC1 using siRNA inhibited cell proliferation, induced apoptosis, and promoted cell migration and invasion. The results of the microarray analysis revealed that the depletion of CLIC1 regulated apoptosis via the TLR2/JNK pathway. Immunohistochemistry showed that CLIC1 was present in the cytoplasm of carcinoma cells, and that the very strong or very weak expression of CLIC1 was an independent poor prognostic factor. Conclusion The present results suggest that the very strong expression of CLIC1 enhances tumor survival, while its very weak expression promotes cellular movement. The present study provides an insight into the role of CLIC1 as a switch among tumor behaviors in ESCC. Disclosure All authors have declared no conflicts of interest.

scholarly journals LncRNA GHET1 Promotes Esophageal Squamous Cell Carcinoma Cells Proliferation and Invasion via Induction of EMT

2017 ◽  
Vol 32 (4) ◽  
pp. 403-408 ◽  
Author(s):  
Hongfen Liu ◽  
Qiang Zhen ◽  
Yakun Fan
Keyword(s):  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Noncoding Rna ◽  
In Vitro Assays ◽  
Migration And Invasion ◽  
Advanced Tumor

Background Recent studies have shown that long noncoding RNA (IncRNA) gastric carcinoma highly expressed transcript 1 (GHET1) was involved in the progression of tumors. However, the role of GHET1 in esophageal squamous cell carcinoma (ESCC) remains unclear. Methods The expression of IncRNA GHET1 was examined in 55 paired ESCC tissues and adjacent nontumor tissues. Molecular and cellular techniques were used to explore the role of GHET1 on ESCC cells. Results Our data showed that GHET1 expression was significantly increased in ESCC tissues and cell lines. High GHET1 expression in ESCC tissues was significantly associated with poor differentiation, advanced tumor nodes metastasis stage, and lymph node metastasis. GHET1 showed high sensitivity and specificity for diagnosing ESCC. Our data from in vitro assays showed that GHET1 inhibition suppressed ESCC cells proliferation, migration, and invasion, and induced cells apoptosis. Furthermore, western blot showed that GHET1 inhibition significantly decreased the expression of vimentin and N-cadherin while it increased the expression of E-cadherin. Conclusions Our study indicates that GHET1 acts as an oncogene in ESCC and may represent a novel therapeutic target for the treatment of ESCC patients.

scholarly journals The Role of Collagen XVII in Cancer: Squamous Cell Carcinoma and Beyond

2020 ◽  
Vol 10 ◽  
Author(s):  
Virginia A. Jones ◽  
Payal M. Patel ◽  
Frederick T. Gibson ◽  
Adriana Cordova ◽  
Kyle T. Amber
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Collagen Xvii
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