scholarly journals Role of miR‐218‐GREM1 axis in epithelial‐mesenchymal transition of oral squamous cell carcinoma: An in vivo and vitro study based on microarray data

2020 ◽  
Vol 24 (23) ◽  
pp. 13824-13836
Author(s):  
Yanpeng Wang ◽  
Yifeng Jiang ◽  
Long Chen
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Microarray Data ◽  
Epithelial Mesenchymal Transition ◽  
Vitro Study ◽  
Mesenchymal Transition

scholarly journals Aberrant Expression and Subcellular Localization of PER2 Promote the Progression of Oral Squamous Cell Carcinoma

2020 ◽  
Vol 2020 ◽  
pp. 1-10
Author(s):  
Fengyuan Guo ◽  
Qingming Tang ◽  
Guangjin Chen ◽  
Jiwei Sun ◽  
Junyi Zhu ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Subcellular Localization ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Epithelial Mesenchymal Transition ◽  
Aberrant Expression ◽  
Mesenchymal Transition

Oral squamous cell carcinoma, one of the most prevalent cancer types in the world, has been confirmed under the influence of a key circadian gene, PER2, whose role has been identified in the development of some other types of cancers. However, the mechanism through which PER2 regulates the progress of OSCC remains largely unknown. In this study, we showed that besides the abnormal expression and subcellular localization of PER2 observed in OSCC tissues and cells as expected, these anomalous changes also existed in the adjacent noncancerous tissues, which was a novel finding in our research. The phase of PER2 rhythmic expression pattern in OSCC cells was later than that in oral keratinocytes in the protein level. In addition, we demonstrated that PER2 played as a resistant factor in the development of OSCC by upregulating TP53 and inhibiting epithelial-mesenchymal transition in vitro and in vivo. Taken together, our results identified that the development of OSCC is closely associated with PER2, the aberrant expression and subcellular localization of which facilitates the malignant progress.

Iroquois Homeobox 5 Negatively Regulated by miRNA-147 Promotes the Proliferation, Metastasis, and Invasion by Oral Squamous Cell Carcinoma

2021 ◽  
Vol 17 (6) ◽  
pp. 1098-1108
Author(s):  
Ziyu Zhu ◽  
Jiaxing Gong ◽  
Jianlu Kong ◽  
Ying Qian ◽  
Kejie Lu ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Epithelial Mesenchymal Transition ◽  
Malignant Tumors ◽  
Cell Multiplication ◽  
Promoting Effect ◽  
Mesenchymal Transition

Oral squamous cell carcinoma (OSCC) is one of the most common tumors worldwide and has one of the highest mortalities. The progression of OSCC is accompanied by changes in the levels of many genes. Iroquois homeobox 5 (IRX5), a novel protein involved in several embryonic developmental processes, has been found in recent years to play a significant role in regulating the growth of malignant tumors. However, its role and mechanism in OSCC are still unclear. In this study, we used nano-PCR to examine the levels of IRX5 in OSCC tissues. Through overexpression and knockdown experiments, we researched the role of IRX5 in regulating OSCC cell multiplication, metastasis, and epithelial-mesenchymal transition (EMT). The results demonstrated that IRX5 expression is higher in OSCC tissues in contrast to adjacent tissues. Overexpression of IRX5 promotes the multiplication, metastasis, invasion, and EMT of OSCC cells. Additional bioinformatics analysis showed that miRNA-147 can target the 3’UTR end of IRX5 and negatively regulate its expression, and overexpression of miRNA-147 can weaken the cancer-promoting effect of IRX5. In conclusion, this study found that IRX5 plays a role in promoting cancer in OSCC, and IRX5 is also negatively regulated by miRNA-147.

scholarly journals The Oncogenic Activity of miR-29b-1-5p Induces the Epithelial-Mesenchymal Transition in Oral Squamous Cell Carcinoma

2019 ◽  
Vol 8 (2) ◽  
pp. 273 ◽  
Author(s):  
Miyako Kurihara-Shimomura ◽  
Tomonori Sasahira ◽  
Hiroyuki Shimomura ◽  
Chie Nakashima ◽  
Tadaaki Kirita
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Epithelial Mesenchymal Transition ◽  
Histological Grade ◽  
Oral Epithelium ◽  
Mesenchymal Transition ◽  
The Relationship

Background: The relationship between miR-29b-1-5p and c-Met proto-oncogene in oral squamous cell carcinoma (OSCC) remains to be investigated. This study aimed to reveal the role of miR-29b-1-5p in the pathogenesis of OSCC using molecular and biological analyses. Methods: We investigated the expression of miR-29b-1-5p, c-Met, and markers of the epithelial-mesenchymal transition (EMT) in the tissues of 49 patients with OSCC and in human OSCC cells with different tumorigenicity. Further, we determined the effects of miR-29b-1-5p on the phenotypes of OSCC cell lines. Results: The expression levels of miR-29b-1-5p in most patients with OSCC were higher than those of the normal oral epithelium. In OSCC, upregulation of miR-29b-1-5p significantly correlated with histological grade, the EMT, and the immunohistochemical grade, indicated by c-Met expression. The prognosis was poor for patients with miR-29b-1-5p expression and coexpression of miR-29b-1-5p and c-Met. In OSCC cells exhibiting the EMT phenotype, knockdown of miR-29b-1-5p suppressed the EMT, which was recovered by enforced expression of c-Met. Further, the mRNA encoding cadherin 1 (CDH1) was a direct target of miR-29b-1-5p. Conclusions: Our results suggest that miR-29b-1-5p acts as an oncogenic miRNA that synergizes with c-Met to induce the EMT of OSCC cells.

scholarly journals Ephrin A4-ephrin receptor A10 signaling promotes cell migration and spheroid formation by upregulating NANOG expression in oral squamous cell carcinoma cells

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Yu-Lin Chen ◽  
Yi-Chen Yen ◽  
Chuan-Wei Jang ◽  
Ssu-Han Wang ◽  
Hsin-Ting Huang ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Migration ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Epithelial Mesenchymal Transition ◽  
Mesenchymal Transition ◽  
Promising Therapeutic Approach ◽  
Sphere Formation

AbstractEphrin type-A receptor 10 (EPHA10) has been implicated as a potential target for breast and prostate cancer therapy. However, its involvement in oral squamous cell carcinoma (OSCC) remains unclear. We demonstrated that EPHA10 supports in vivo tumor growth and lymphatic metastasis of OSCC cells. OSCC cell migration, epithelial mesenchymal transition (EMT), and sphere formation were found to be regulated by EPHA10, and EPHA10 was found to drive expression of some EMT- and stemness-associated transcription factors. Among EPHA10 ligands, exogenous ephrin A4 (EFNA4) induced the most OSCC cell migration and sphere formation, as well as up-regulation of SNAIL, NANOG, and OCT4. These effects were abolished by extracellular signal-regulated kinase (ERK) inhibition and NANOG knockdown. Also, EPHA10 was required for EFNA4-induced cell migration, sphere formation, and expression of NANOG and OCT4 mRNA. Our microarray dataset revealed that EFNA4 mRNA expression was associated with expression of NANOG and OCT4 mRNA, and OSCC patients showing high co-expression of EFNA4 with NANOG or OCT4 mRNA demonstrated poor recurrence-free survival rates. Targeting forward signaling of the EFNA4-EPHA10 axis may be a promising therapeutic approach for oral malignancies, and the combination of EFNA4 mRNA and downstream gene expression may be a useful prognostic biomarker for OSCC.

scholarly journals FAP overexpression induce Epithelial-Mesenchymal Transition (EMT) in oral squamous cell carcinoma by down-regulating DPP9 gene

2019 ◽  
Author(s):  
Qing-qing Wu ◽  
Meng Zhao ◽  
Guang-zhao Huang ◽  
Ze-nan Zheng ◽  
Wei-sen Zeng ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Epithelial Mesenchymal Transition ◽  
Tumor Promoter ◽  
Tissue Samples ◽  
Mesenchymal Transition

AbstractFAP acts as a tumor promoter via epithelial-mesenchymal transition (EMT) in human oral squamous cell carcinoma (OSCC). The present study was designed to investigate the interaction proteins with FAP and explore the precise mechanism of FAP promoting EMT in OSCC. IP-MS analysis confirmed that DPP9 was an interacting protein of FAP. DPP9 was down-regulated in OSCC tissue samples compared with MNT using immunohistochemistry and quantitative-PCR detection. Lower DPP9 was correlated with unfavorable overall survival of patients with OSCC. Repressing DPP9 accelerates the proliferation of OSCC cells in vitro and in vivo. Mechanistically, overexpression of FAP downregulate the expression of the DPP9 and the effect of FAP on OSCC proliferation, migration, invasion and EMT could be reversed by up-regulated DPP9. Our study suggests that FAP could induce EMT and promote carcinogenesis in oral squamous cell carcinoma by down-regulating DPP9 gene. That will hint different dimension on therapy for patients with OSCC.

scholarly journals CCL18-induced LINC00319 promotes proliferation and metastasis in oral squamous cell carcinoma via the miR-199a-5p/FZD4 axis

2020 ◽  
Vol 11 (9) ◽  
Author(s):  
Xiao Jiang ◽  
Jingpeng Liu ◽  
Simin Li ◽  
Bo Jia ◽  
Zhijie Huang ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Epithelial Mesenchymal Transition ◽  
Mesenchymal Transition ◽  
In Vivo Experiments ◽  
Oral Cancer Cells

Abstract Long non-coding RNAs (lncRNAs), which may be modulated by chemokines, are key regulators in many cancers including oral squamous cell carcinoma (OSCC). An understanding of lncRNAs involved in chemokine (CC motif) ligand 18 (CCL18)-induced OSCC promotion remains elusive. The present study using lncRNA sequencing found LINC00319 to be significantly upregulated in OSCC cells subjected to rCCL18 stimulation. Furthermore, LINC00319 knockdown was found to attenuate the carcinogenic function of CCL18 in OSCC, reducing OSCC proliferation, metastasis, epithelial-mesenchymal transition (EMT), and angiogenesis. LINC00319 was demonstrated to act as a ceRNA in OSCC, which directly responded to miR-199a-5p and rescued the repression of FZD4 by miR-199a-5p. Functionally, in vitro and in vivo experiments showed that LINC00319 promoted OSCC growth and metastasis via downregulating miR-199a-5p and upregulating FZD4. In vitro rescue assays demonstrated that miR-199a-5p inhibitor or FZD4 overexpression reversed the effects of LINC00319 silencing in OSCC. Importantly, the expression of miR-199a-5p and FZD4 were found to be mediated by CCL18, and miR-199a-5p mimics inhibited the CCL18-promoting effects in oral cancer cells. Taken together, these results evidenced a mechanism of CCL18 action in OSCC mediated through the LINC00319/miR-199a-5p/FZD4 signaling pathway, which may comprise a potential target for OSCC therapeutic development.

scholarly journals FGF8 induces epithelial-mesenchymal transition and promotes metastasis in oral squamous cell carcinoma

2020 ◽  
Author(s):  
Yilong Hao ◽  
rui liu
Keyword(s):  
Squamous Cell Carcinoma ◽  
Growth Factors ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Epithelial Mesenchymal Transition ◽  
Mechanistic Study ◽  
Therapeutic Effects ◽  
Mesenchymal Transition

Abstract Background Oral squamous cell carcinoma (OSCC) is one of the most common cancers worldwide, and with 500,000 new cases each year. The high risk of lymph node metastasis and local invasion are the main causes to cripples and death of OSCC patients. As potent growth factors, fibroblast growth factors (FGFs) not only exert biological effects for primary epithelial cells, but also make FGF signaling susceptible to being hijacked by cancer cells. However, the precise role of FGF8 and the therapeutic effects of FGF8 in OSCC need to be further investigated. Methods Immunohistochemical staining was performed using in human OSCC tissues. Bioinformatics analysis was performed to analyze the potential FGF8-associated proteins. Migration and invasion of OSCC cells was examined by wounding healing assay and Matrigel assay. Expression of EMT related markers Was examined by immunoblot. Results In this study, we show that FGF8 is upregulated in OSCC tissues and high FGF8 expression was related with a set of clinicopathologic parameters, including age, drinking, and survival time. FGF8 treatment enhances the invasive capability of OSCC cells. Lentivirus-based FGF8 expression promotes OSCC metastasis in a mouse lung metastasis model. Further, mechanistic study demonstrated that FGF8 induces epithelial-mesenchymal transition in OSCC cells. Conclusions These results highlight a pro-metastatic role of FGF8, and underscore the role of FGF8 in OSCC development.

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