scholarly journals miR-424-5p Promotes Proliferation, Migration and Invasion of Laryngeal Squamous Cell Carcinoma

2019 ◽  
Vol Volume 12 ◽  
pp. 10441-10453 ◽  
Author(s):  
Yujun Li ◽  
Jie Liu ◽  
Wanglai Hu ◽  
Yuliang Zhang ◽  
Jiangwei Sang ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Laryngeal Squamous Cell Carcinoma ◽  
Migration And Invasion

Interferon-induced transmembrane protein 1 (IFITM1) is essential for progression of laryngeal squamous cell carcinoma in an Osteopontin/NF-κB-dependent manner

2020 ◽  
Vol 29 (4) ◽  
pp. 521-529
Author(s):  
Yong Yin ◽  
Keke Yang ◽  
Juanjuan Li ◽  
Peng Da ◽  
Zhenxin Zhang ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Signaling Pathway ◽  
Squamous Cell ◽  
Laryngeal Squamous Cell Carcinoma ◽  
Transmembrane Protein ◽  
Migration And Invasion ◽  
Dependent Manner ◽  
Tissue Samples ◽  
Normal Tissues

OBJECTIVE: To assess the expression levels of IFITM1 in human tissue samples and laryngeal squamous cell carcinoma (LSCC) cells, and to explore the potential mechanisms of IFITM1 in LSCC progression. METHODS: Quantitative PCR and immunohistochemical (IHC) assays were performed to detect IFITM1 expression in 62 LSCC tissues and corresponding normal tissues. We further detected the effects of IFITM1 on the proliferation, migration and invasion of LSCC cells and NF-κB signaling pathway through colony formation assay, wound healing assay and transwell assay, respectively. RESULTS: We demonstrated the possible involvement of IFITM1 in the progression of LSCC. We found the upregulated expression of IFITM1 in human LSCC tissues and cells, and analyzed the correlations between IFITM1 expression and osteopontin. Our data further confirmed that IFITM1 affected cell proliferation, migration, and invasion of LSCC cells via the regulation of NF-κB signaling pathway. CONCLUSIONS: We investigated the potential involvement of IFITM1 in the progression of LSCC, and therefore confirmed that IFITM1 was a potential therapeutic target for LSCC.

scholarly journals LncRNA TM4SF19-AS1 Promotes the Proliferation, Migration and Invasion of Laryngeal Squamous Cell Carcinoma by Targeting miR-153-3p/ITGAV Axis

2021 ◽  
Author(s):  
Yudong Liu ◽  
Xiaojuan Feng ◽  
Yuexin Tian ◽  
Yanzhuo Zhang ◽  
Huan Cao ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Laryngeal Squamous Cell Carcinoma ◽  
Subcellular Location ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Tissue Samples ◽  
Node Metastasis ◽  
Dual Luciferase Reporter Assay

Abstract Background: LncRNA plays an important role in the gene regulatory network and can affect the progress of tumors. LncRNA TM4SF19-AS1 has been reported may associate with the occurrence and development of head and neck squamous cell carcinoma. Methods: LncRNA TM4SF19-AS1 expression in laryngeal squamous cell carcinoma (LSCC) tissue samples was evaluated in TCGA database, and its expression in LSCC tissues and cells was further determined via qRT-PCR. CCK-8, EdU, wound healing and transwell assays were performed to access the cell biological behaviors of TM4SF19-AS1. The downstream regulatory mechanism of TM4SF19-AS1 regulating gene expression was further detected by WGCNA, subcellular location prediction, western blot and dual-luciferase reporter assay.Results: The expression of TM4SF19-AS1 was upregulated in LSCC tissues and positively correlated with tumor-node-metastasis (TNM) stage and lymph node metastasis in LSCC patients. Knockdown of TM4SF19-AS1 suppressed the proliferation, migration and invasion of LSCC cells. Mechanistically, TM4SF19-AS1 acted as a competing endogenous RNA (ceRNA) that directly bound to miR-153-3p, and ITGAV was the direct target of miR-153-3p.Conclusions: LncRNA TM4SF19-AS1 promotes the proliferation, migration and invasion of laryngeal carcinoma by targeting miR-153-3p/ITGAV axis, suggesting that TM4SF19-AS1 could be a potential diagnostic biomarker and an effective target for the treatment for LSCC.

scholarly journals MicroRNA-625 inhibits cell invasion and epithelial–mesenchymal transition by targeting SOX4 in laryngeal squamous cell carcinoma

2019 ◽  
Vol 39 (1) ◽  
Author(s):  
Yuan Li ◽  
Chenjuan Tao ◽  
Lili Dai ◽  
Caixia Cui ◽  
Chaohui Chen ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Laryngeal Squamous Cell Carcinoma ◽  
Critical Role ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Mesenchymal Transition ◽  
Expression Levels

AbstractIntroduction: Laryngeal squamous cell carcinoma (LSCC) is a highly aggressive malignant cancer, but the molecular mechanisms underlying its development and progression remain largely elusive. The purpose of the present study is to investigate the expression profile and functional role of microRNA-625 (miR-625) in LSCC.Materials and methods: LSCC tissues and adjacent normal tissues were collected from 86 LSCC patients. The expression levels of miR-625 and SOX4 mRNA in tissues and cells were detected by RT-qPCR analysis. The expression levels of SOX4 and EMT-related proteins were detected by western blot analysis. In vitro cell proliferation, migration, and invasion were detected by MTT assay, colony formation assay, wound healing assay, and transwell invasion assay, respectively. Dual-luciferase reporter assay was performed to verify the binding relationship between miR-625 and the 3′-UTR of SOX4.Results: The results demonstrated that miR-625 is significantly down-regulated in clinical LSCC tissues, and its low expression may be closely associated with unfavorable clinicopathological characteristics of LSCC patients. Overexpression of miR-625 significantly suppressed the proliferation, migration, invasion, and EMT of LSCC cells. Furthermore, SOX4 was validated as a direct target of miR-625 in LSCC cells, and rescue experiments suggested that restoration of SOX4 blocked the tumor suppressive role of miR-625 in LSCC cells.Conclusions: Taken together, these findings highlighted a critical role of miR-625 in the pathogenesis of LSCC, and restoration of miR-625 could be considered as a potential therapeutic strategy against this fatal disease.

scholarly journals IQGAP1 silencing suppresses the malignant characteristics of laryngeal squamous cell carcinoma cells

2017 ◽  
Vol 33 (1) ◽  
pp. 73-78 ◽  
Author(s):  
Xiaoxia Wang ◽  
Chun He ◽  
Chaohui Li ◽  
Benhong Ren ◽  
Qing Deng ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Epithelial To Mesenchymal Transition ◽  
Laryngeal Squamous Cell Carcinoma ◽  
Migration And Invasion ◽  
Mesenchymal Transition ◽  
First Time

Background: Laryngeal squamous cell carcinoma (LSCC) has a poor prognosis due to recurrence and metastasis. IQ-domain GTPase-activating protein 1 (IQGAP1), a scaffold protein, plays an important role in tumorigenesis and malignant development. In this study, we aimed to explore the role of IQGAP1 in LSCC. Methods: Expression of IQGAP1 in human LSCC specimens was assessed by immunohistochemistry. We also evaluated the roles of IQGAP1 in cell proliferation, migration and invasion and epithelial-to-mesenchymal transition (EMT) in Hep-2 cells. Results: The expression of IQGAP1 protein was significantly up-regulated in LSCC tissues compared with normal laryngeal tissues (p = 0.002). Furthermore, the knockdown of IQGAP1 in Hep-2 cells inhibited cell growth, migration and invasion. Moreover, we found that IQGAP1 silencing reversed EMT. Conclusions: These results show for the first time that IQGAP1 is up-regulated in LSCC tissues and plays an important role in LSCC cell proliferation and invasiveness, which indicates that IQGAP1 could work as an oncogene and may serve as a promising molecular target for treatment of LSCC.

scholarly journals AlG3 Induces AURKA to Promote Laryngeal Squamous Cell Carcinoma Metastasis

2022 ◽  
Author(s):  
shuixian huang ◽  
Li-Yun YANG ◽  
Peipei Qiao ◽  
An Hu
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Prognostic Value ◽  
Laryngeal Squamous Cell Carcinoma ◽  
Migration And Invasion ◽  
Clinical Prognosis ◽  
Carcinoma Metastasis ◽  
The Impact ◽  
The Relationship

Abstract Objectives To investigate the relationship between ALG3 and AURKA, the expression and potential prognostic value of ALG3 in LSCC, and to then explore the impact of ALG3 in tumorigenic effects.Methods Co-immunoprecipitation assay was detected the relationship between ALG3 and AURKA, Rt-PCR and Western blot was detected the expression of related mRNA and proteins. CCK8 assay, plate colony formation assay Cells, wound healing, migration and invasion assays were used to examine the ability of proliferation, movement, migration and invasion of LSCC cells.Results ALG3 immediately induced AURKA to promote LSCC metastasis. Moreover, ALG3 highly expressed in LSCC tissues and cells and the expression of ALG3 was positively related to tumor size, lymphatic metastasis and poor clinical prognosis. Furthermore, knockdown ALG3 in LSCC cells remarkably restrain cellular proliferation, migration and invasion in vitro and vivo.Conclusion AlG3 induced AURKA to promote LSCC metastasis and ALG3 maybe potential prognostic value for LSCC.Brief AbstractAlG3 induces AURKA to promote laryngeal squamous cell carcinoma metastasis

scholarly journals Efficacy of radiation exposure in laryngeal squamous cell carcinoma is mediated by the LAMP3/LAMC2/tenascin-C pathway

2019 ◽  
Vol 244 (13) ◽  
pp. 1070-1080 ◽  
Author(s):  
Hao Wu ◽  
Juanjuan Li ◽  
Jianqiu Chen ◽  
Yong Yin ◽  
Peng Da ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Radiation Exposure ◽  
Cell Carcinoma ◽  
Signaling Pathways ◽  
Squamous Cell ◽  
Laryngeal Squamous Cell Carcinoma ◽  
Migration And Invasion ◽  
Pdx Model

The present study explored the role of LAMP3 and related molecular mechanisms in the efficacy of radiation exposure in laryngeal squamous cell carcinoma (LSCC). A lentivirus vector containing the LAMP3 gene was transfected into HEp-2 cells to construct siRNA-LAMP3 and complementation (siLAMP3+LAMP3) groups. Treatment with 4 Gy or 8 Gy radiation was administered to evaluate the role of LAMP3 in radiation therapy. Apoptosis was detected by Annexin V/propidium iodide double staining. Cell migration and invasion were measured in vitro using Transwell and Matrigel assays. Downstream genes regulated by LAMP3 were analyzed using RNA sequencing. Furthermore, a patient-derived xenograft (PDX) model of LSCC was established to verify the efficacy of radiation exposure and the associated signaling pathways downstream of LAMP3. The efficacy of radiation showed that cell proliferation was significantly inhibited by siRNA-LAMP3 knockdown. Increased apoptosis was also observed. Notably, the inhibitory effect was attenuated and apoptosis rates were decreased after LAMP3 complementation. In vitro cellular assays showed that migration and invasion were significantly suppressed by siRNA-LAMP3 knockdown and increased after LAMP3 complementation. Analysis of the efficacy of radiation exposure in the PDX model showed that LAMP3-specific knockdown inhibited tumor growth and that tumor growth was further reduced by the combined radiotherapy treatment. According to transcriptome analysis, the extracellular matrix-receptor interaction pathway is regulated by LAMP3, and further analysis revealed significant differences in key-associated molecules, including laminin subunit gamma-2 (LAMC2) and tenascin-C (TNC). Validation of the in vivo PDX model using qPCR and Western blot analyses supported the abovementioned results. The present findings suggest that reduced LAMP3 expression enhances the efficacy of radiation exposure in LSCC by regulating the LAMP3/LAMC2/TNC signaling pathway. Impact statement It is important to establish effective early diagnostic indicators and reliable treatment strategies for laryngeal squamous cell carcinoma (LSCC). We previously found that expression of LAMP3 was significantly higher in cancerous tissues compared to adjacent normal surgical margin tissues. The present study explored the role of LAMP3 and the related molecular mechanisms in the efficacy of radiation exposure in LSCC. In vitro Transwell and Matrigel assays were performed, and a patient-derived xenograft (PDX) model of LSCC was established. Associated signaling pathways downstream of LAMP3 were analyzed using RNA sequencing. Signaling pathways regulated by LAMP3 were clearly identified by combining the PDX model with transcriptome analysis. Reduced LAMP3 expression enhanced the efficacy of radiation exposure in LSCC. Thus, by utilizing this molecule as a marker, specific groups of patients may be screened for targeted therapy in the future.

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