scholarly journals MiR-148a inhibits oral squamous cell carcinoma progression through ERK/MAPK pathway via targeting IGF-IR

2020 ◽  
Vol 40 (4) ◽  
Author(s):  
Tingting Jia ◽  
Yipeng Ren ◽  
Fengze Wang ◽  
Rui Zhao ◽  
Bo Qiao ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Mapk Pathway ◽  
Mapk Signaling ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Node Metastasis ◽  
Erk Mapk

Abstract Objective: The current study aimed to investigate the functional roles and clinical significance of microRNA-148a (miR-148a) in the progression of oral squamous cell carcinoma (OSCC). Methods: Relative expression of miR-148a in OSCC cells and tissues were detected using quantitative real-time polymerase chain reaction (qRT-PCR). Chi-square test was performed to estimate the relationship between miR-148a expression and clinical characteristics of OSCC patients. Cell transfection was carried out using Lipofectamine® 2000. Biological behaviors of tumor cells were detected using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and transwell assays. Bioinformatics analysis and luciferase reporter assay were used to identify the target genes of miR-148a. Protein expression was detected through Western blot analysis. Results: MiR-148a expression was obviously decreased in OSCC tissues and cells, and such down-regulation was closely correlated with lymph node metastasis (P=0.027) and tumor node metastasis (TNM) stage (P=0.001) of OSCC patients. miR-148a overexpression could significantly impair OSCC cell proliferation, migration and invasion in vitro (P<0.05 for all). Insulin-like growth factor-I receptor (IGF-IR) was a potential target of miR-148a. MiR-148a could inhibit ERK/MAPK signaling pathway through targeting IGF-IR. Conclusion: MiR-148a plays an anti-tumor role in OSCC and inhibits OSCC progression through suppressing ERK/MAPK pathway via targeting IGF-IR.

scholarly journals Knockdown of circ_0011946 targets miR-216a-5p/BCL2L2 axis to regulate proliferation, migration, invasion and apoptosis of oral squamous cell carcinoma cells

BMC Cancer ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Ying Zhou ◽  
Shuhong Zhang ◽  
Zhonghan Min ◽  
Zhongwei Yu ◽  
Huaiwei Zhang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Tumor Growth ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
B Cell Lymphoma ◽  
Luciferase Reporter ◽  
Migration And Invasion

Abstract Background Circular RNAs (circRNAs) are implicated in the development of oral squamous cell carcinoma (OSCC). The aim of current research is to elucidate the role and mechanism of circ_0011946 in the functional behaviors of OSCC cells. Methods Circ_0011946, microRNA (miR)-216a-5p, B cell lymphoma-2-like 2 protein (BCL2L2) abundances were exposed by quantitative reverse transcription polymerase chain reaction (qRT-PCR) or western blot. Cell proliferation, migration, invasion and apoptosis were detected by MTT, colony formation assay, transwell, wound-healing and flow cytometry assays, respectively. Target correlation was tested by dual-luciferase reporter and RNA pull-down assays. An in vivo xenograft experiment was employed to investigate the function of circ_0011946 on tumor growth in vivo. Results Circ_0011946 and BCL2L2 levels were increased, while miR-216a-5p level was decreased in OSCC tissues and cells. Circ_0011946 knockdown impeded proliferation, migration, and invasion, but promoted apoptosis in OSCC cells. Circ_0011946 functioned as a sponge for miR-216a-5p, and BCL2L2 was targeted by miR-216a-5p. Besides, miR-216a-5p or BCL2L2 knockdown partly attenuated the inhibitory influences of circ_0011946 silence or miR-216a-5p overexpression on OSCC cell progression. Furthermore, circ_0011946 post-transcriptionally regulated BCL2L2 through sponging miR-216a-5p. Moreover, circ_0011946 knockdown constrained OSCC tumor growth in vivo. Conclusion Circ_0011946 silence repressed OSCC cell proliferation, migration, and invasion, but promoted apoptosis through the regulation of the miR-216a-5p/BCL2L2 axis.

scholarly journals NF-κB-Mediated lncRNA AC007271.3 as A ceRNA Promotes Carcinogenesis of Oral Squamous Cell Carcinoma by Regulating Slug

2020 ◽  
Author(s):  
Ze-nan Zheng ◽  
Guang-zhao Huang ◽  
Qing-qing Wu ◽  
Heng-yu Ye ◽  
Wei-sen Zeng ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Core Promoter ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Mrna Levels ◽  
E Cadherin

Abstract Background: Oral squamous cell carcinoma (OSCC) is the most common oral cancer. Our previous studies confirmed that dysregulation function of long non-coding RNA (lncRNA) AC007271.3 was associated with a poor prognosis and overexpression of AC007271.3 promoted cell proliferation, migration, invasion and inhibited cell apoptosis in vitro, and promoted tumor growth in vivo. However, the underlying mechanisms of AC007271.3 dysregulation remained obscure.Methods: Bioinformatics databases were used to predicted the potential down-stream targeted of AC007271.3 and verified by dual luciferase reporter assay. Core promoter region of AC007271.3 was identified by luciferase activity assay and the potential transcription factor on it was verified by ChIP assay. Western blot and qRT-PCR were performed to detect the protein and messenger RNA (mRNA) levels, respectively. Animal experiments confirmed the metastatic ability in vivo.Results: AC007271.3 functioned as competing endogenous RNA (ceRNA) by binding to miR-125b-2-3p and upregulated the expression of Slug, which is a direct target of miR-125b-2-3p. AC007271.3 enhanced the expression of Slug and inhibited the expression of E-cadherin to promote the migration and invasion in OSCC cells. The expression of AC007271.3 was promoted by canonical nuclear factor-κB (NF-κB) pathway. Conclusion: Our study showed that the classical NF-κB pathway-activated AC007271.3 regulates EMT by miR-125b-2-3p / Slug / E-cadherin axis to promote the development of OSCC, implicating it as a novel potential target for therapeutic intervention in this disease.

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.

LncRNA MCM3AP-AS1 promotes proliferation, migration and invasion of oral squamous cell carcinoma cells via regulating miR-204-5p/FOXC1

2020 ◽  
Vol 68 (7) ◽  
pp. 1282-1288
Author(s):  
Hui Li ◽  
Junhong Jiang
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Molecular Mechanisms ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Qrt Pcr ◽  
Gene Assay

Oral squamous cell carcinoma (OSCC) is a lethal malignancy. It is reportedly demonstrated that long non-coding RNA (lncRNA) participates in the development of OSCC. The purpose of this study was to clarify the function and possible molecular mechanisms of lncRNA MCM3AP antisense RNA 1 (lncRNA MCM3AP-AS1) in OSCC. Quantitative real-time PCR (qRT-PCR) was adopted to investigate MCM3AP-AS1 expressions in OSCC tissues and cells. The proliferation, migration and invasion of HN-6 and SCC-9 cells were probed by cell counting kit-8 and Transwell assays, respectively. Dual luciferase reporter gene assay, Pearson’s correlation analysis, qRT-PCR and western blot were used to detect the binding relationship among miR-204-5 p, MCM3AP-AS1 and forkheadbox C1 (FOXC1). MCM3AP-AS1 expression was elevated in OSCC tissues and cell lines. Overexpression of MCM3AP-AS1 facilitated the proliferation, migration and invasion of OSCC cells, while the knockdown of MCM3AP-AS1 suppressed these malignant phenotypes. Besides, MCM3AP-AS1 impeded miR-204-5 p by binding with it. MCM3AP-AS1 could also upregulate the expression of FOXC1 via repressing miR-204-5 p.MCM3AP-AS1 promotes the progression of OSCC cells by adsorbing miR-204-5 p and upregulating FOXC1 expressions.

Knockdown of Nav1.5 inhibits cell proliferation, migration and invasion via Wnt/β-catenin signaling pathway in oral squamous cell carcinoma

2020 ◽  
Vol 52 (5) ◽  
pp. 527-535 ◽  
Author(s):  
Xiaoli Xu ◽  
Yongzheng Dai ◽  
Linfei Feng ◽  
Hongli Zhang ◽  
Yukun Hu ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Signaling Pathway ◽  
Squamous Cell ◽  
Migration And Invasion ◽  
High Recurrence Rate ◽  
Lymphocyte Ratio ◽  
Node Metastasis ◽  
Tumor Node Metastasis Stage

Abstract Oral squamous cell carcinoma (OSCC) is a common type of malignant oral cancer that has a high recurrence rate. Voltage-gated sodium channel Nav1.5 was reported to be highly up-regulated in various types of cancers. However, the regulatory mechanism of Nav1.5 in cancers including OSCC still remains elusive. In this study, Nav1.5 was found to be highly expressed in OSCC tissues and cells. Through the analysis of clinical characteristics of patients, we found that the expression level of Nav1.5 was closely related to neutrophil-to-lymphocyte ratio, platelet-to-lymphocyte ratio, tumor-node-metastasis stage, and lymph node metastasis. Moreover, we found that Nav1.5 mainly located on the cell membrane as well as cytoplasm and knockdown of Nav1.5 promoted cell apoptosis and decreased proliferation in OSCC. Transwell assay results showed that knockdown of Nav1.5 effectively suppressed the migration and invasion in OSCC. In addition, knockdown of Nav1.5 was found to inhibit the protein and mRNA expression levels of β-catenin, cyclin D1, and c-Myc in the Wnt/β-catenin signaling pathway. In summary, these results indicated that Nav1.5 may be involved in the progression of OSCC through the Wnt/β-catenin signaling pathway.

scholarly journals MicroRNA-99a-5p suppresses cell proliferation, migration, and invasion by targeting isoprenylcysteine carboxylmethyltransferase in oral squamous cell carcinoma

2021 ◽  
Vol 49 (5) ◽  
pp. 030006052093903
Author(s):  
Xiang Sun ◽  
Huixin Yan
Keyword(s):  
Cell Proliferation ◽  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Cell Lines ◽  
Squamous Cell ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Isoprenylcysteine Carboxylmethyltransferase

Background MicroRNA (miR)-99a-5p acts as a tumor suppressor in several tumors, including bladder cancer and breast cancer, but its biological function in oral squamous cell carcinoma (OSCC) is poorly understood. Methods miR-99a-5p expression was determined in OSCC tissues and cell lines using quantitative reverse transcription polymerase chain reaction (RT-qPCR). Cell proliferation was assessed by the Cell Counting Kit-8 assay and colony formation assay. Wound healing and Transwell assays were used to analyze migration and invasion abilities, respectively, in OSCC cells. The luciferase reporter assay, RT-qPCR, and western blotting were used to determine the relationship between miR-99a-5p and isoprenylcysteine carboxylmethyltransferase (ICMT). Results miR-99a-5p expression in OSCC tissues and cell lines was significantly decreased compared with corresponding controls, and was significantly associated with clinical stage and lymph node metastasis in OSCC. Functional assays revealed that miR-99a-5p overexpression significantly inhibited the proliferation, migration, and invasion abilities of CAL-27 and TCA-8113 OSCC cells. miR-99a-5p was found to directly target ICMT, while ICMT restoration reversed the role of miR-99a-5p in OSCC cells. Conclusions Our results indicate that miR-99a-5p-mediates the down-regulation of ICMT, which could be used as a novel potential therapeutic target for OSCC treatment.

scholarly journals Circ_0005232 Promotes the Progression of Oral Squamous Cell Carcinoma by Sponging miR-1299 to Regulate CDK6

2021 ◽  
Author(s):  
Xue Zhang ◽  
Guang-Yu Guo ◽  
Zhen-Hua Wang ◽  
Zhong-Ti Zhang
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Cell Lines ◽  
Squamous Cell ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Mesenchymal Transition ◽  
Qrt Pcr ◽  
Rna Immunoprecipitation

Abstract Objectives: CircRNA may play essential roles and act as biomarkers in tumor development due to their special stable structure. However, the mechanism by which circRNAs affect OSCC progression is still unclear. Methods: qRT-PCR was performed to detect circ_0005232 expression level in oral squamous cell carcinoma (OSCC) tissues and cell lines. Colony formation assays, cell migration and invasion assays, and wound healing assays were performed to verify the effects of overexpression or knockdown of circ_0005232 on the biological function of OSCC cell lines. Western blot was performed to determine the effects of circ_0005232 on epithelial-to-mesenchymal transition (EMT) and expression of MMP2 and MMP9 in OSCC cell lines. Dual luciferase reporter assays, rescue assays, RNA immunoprecipitation assays, and EDU incorporation assays were performed to explore interactions among circ_0005232, miR-1299, and CDK6. Results: qRT-PCR results confirmed that circ_0005232 was expressed significantly higher in OSCC tissue and cell lines. Functional experiments indicated that overexpression of circ_0005232 promoted OSCC cell lines proliferation，migration and invasion ability, while inhibition of circ_0005232 caused opposite results. MiR-1299 knockdown could rescue the changes in cell function caused by circ_0005232 knockdown. The dual luciferase reporter assay verified that circ_0005232 could bind with miR-1299 to affect the proliferation，migration and invasion ability of OSCC cell lines. RNA immunoprecipitation assays indicated that circ_0005232 could increase CDK6 expression by sponging miR-1299.Conclusions: Our results demonstrate that circ_0005232 exerts its tumor-promoting effects by sponging miR-1299 which then affects function of CDK6. Therefore, circ_0005232 may represent a novel potential prognostic biomarker and therapeutic target in OSCC.

scholarly journals miRNA-101 Targets TGF-βR1 to Retard the Progression of Oral Squamous Cell Carcinoma

2020 ◽  
Vol 28 (2) ◽  
pp. 203-212 ◽  
Author(s):  
Yong Wang ◽  
Rui-Zhi Jia ◽  
Shu Diao ◽  
Jun He ◽  
Li Jia
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Transforming Growth Factor ◽  
Ectopic Expression ◽  
Transforming Growth Factor Β ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Migration And Invasion

Despite the considerable knowledge on the involvement of microRNA-101 (miR-101) in the evolution of oral squamous cell carcinoma (OSCC), the underlying mechanisms remain obscure. In this study, miR-101 expression was markedly downregulated in the OSCC cell lines and tissues. Cell counting kit-8 (CCK-8), ethynyl deoxyuridine (EdU), and colony formation assays showed that miR-101 inhibited the proliferation of OSCC cells. Flow cytometry and caspase 3 activity assays indicated that miR-101 induced OSCC cell apoptosis. Transwell assays demonstrated that this miRNA also repressed OSCC cell migration and invasion. Moreover, tube formation assay showed that miR-101 abated the proangiogenesis of OSCC cells. Dual-luciferase reporter assay confirmed that miR-101 directly targeted transforming growth factor-β receptor 1 (TGF-βR1) in OSCC. Ectopic expression of TGF-βR1 counteracted the effects of miR-101 on the OSCC cell characteristics. Thus, miR-101 significantly abolished the proliferation, motility, and proangiogenesis of OSCC cells and induced their apoptosis by targeting TGF-βR1. These results imply the potential application of miR-101 in OSCC treatment.

scholarly journals MicroRNA-155-5p Contributes to 5-Fluorouracil Resistance Through Down-Regulating TP53INP1 in Oral Squamous Cell Carcinoma

2021 ◽  
Author(s):  
Bowen Liu ◽  
Jingchao Hu ◽  
Han Zhao ◽  
Li Zhao
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Ectopic Expression ◽  
Expression Level ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Reporter Assay ◽  
Tumor Bearing

Abstract The anticancer drug 5-fluorouracil (5-FU) resistance is a major obstacle to reducing the effectiveness of cancer treatment, and its detailed mechanism has not been fully elucidated. Here, in 5-FU-resistant human oral squamous cell carcinoma (OSCC) HSC3 cells (HSC3/5-FU), the levels of 21 miRNA candidates were detected and miR-155-5p level increased strikingly in HSC3/5-FU cells compared to HSC3 cells. Compared with HSC3 cells, the HSC3/5-FU cells transfected with miR-155-5p inhibitors decreased 5-FU IC50. Ectopic expression of miR-155-5p in HSC3 and HSC4 cells increased 5-FU IC50, migration and invasion abilities. Seven miR-155-5p target candidates were discovered by miRNA prediction algorithms, and in HSC3/5-FU cells TP53INP1 showed the lowest mRNA expression level compared with HSC3 cells. Ectopic expression of miR-155-5p in HSC3 and HSC4 cells decreased TP53INP1 expression level, and luciferase reporter assay further determined the interference effect of miR-155-5p on TP53INP1 expression. The enhancement of cell viability, migration and invasion by miR-155-5p after 5-FU treatment was reversed by TP53INP1 overexpression. After treatment with 5-FU, HSC3-miR-155-5p tumor-bearing nude mice presented growing tumors, while HSC3-TP53INP1 group possessed shrinking tumors. In conclusion, these results lead to the proposal that miR-155-5p enhances 5-FU resistance by decreasing TP53INP1 expression in OSCC.

LncRNA SNHG17 promotes the progression of oral squamous cell carcinoma by modulating miR-375/PAX6 axis

2020 ◽  
pp. 1-12
Author(s):  
Fei Tong ◽  
Jun Guo ◽  
Zhanqi Miao ◽  
Zhihua Li
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Regulatory Function ◽  
Migration And Invasion ◽  
Clinical Samples

BACKGROUND: The prognosis of patients with recurrent and/or metastatic oral squamous cell carcinoma (OSCC) remains poor, and its incidence is especially high in developing countries. Multiple long non-coding RNAs (lncRNAs) are recently identified as crucial oncogenic factors or tumor suppressors. This study aimed to probe into the role of lncRNA small nucleolar RNA host gene 17 (SNHG17) on the progression of OSCC. METHODS: The expression level of SNHG17 in OSCC samples was tested using quantitative real-time polymerase chain reaction (qRT-PCR). Human OSCC cell lines CAL-27 and Tca8113 were used in in vitro studies. Cell counting kit-8 (CCK-8) and BrdU assays were used to assess the effect of SNHG17 on OSCC cell proliferation. Flow cytometry was used to study the effect of SNHG17 on OSCC cell apoptosis. Transwell assay was conducted to detect the effect of SNHG17 on migration and invasion. Moreover, luciferase reporter assay was employed to confirm targeting relationship between miR-375 and SNHG17. Additionally, Western blot was used to observe the regulatory function of SNHG17 on PAX6. RESULTS: SNHG17 expression in OSCC clinical samples was significantly increased and was correlated with unfavorable pathological indexes. Its overexpression remarkably accelerated proliferation and metastasis of OSCC cells, while reduced apoptosis. Accordingly, knockdown of SNHG17 suppressed the malignant phenotypes of OSCC cells. Overexpression of SNHG17 significantly reduced the expression of miR-375 by sponging it, but enhanced the expression of PAX6. CONCLUSION: SNHG17 is a sponge of tumor suppressor miR-375 in OSCC, enhances the expression of PAX6 indirectly, and functions as an oncogenic lncRNA.

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