scholarly journals Circ_0058106 promotes proliferation, metastasis and EMT process by regulating Wnt2b/β-catenin/c-Myc pathway through miR-185-3p in hypopharyngeal squamous cell carcinoma

2021 ◽  
Vol 12 (11) ◽  
Author(s):  
Ce Li ◽  
Wenming Li ◽  
Shengda Cao ◽  
Jianing Xu ◽  
Ye Qian ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Hypopharyngeal Cancer ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Hypopharyngeal Carcinoma ◽  
Carcinogenic Effect ◽  
Hypopharyngeal Squamous Cell Carcinoma ◽  
Qrt Pcr

AbstractHypopharyngeal squamous cell carcinoma (HSCC) accounts 95% of hypopharyngeal cancer, which is characterized by high early metastasis rate and poor prognosis. It is reported that circular RNA is involved in the occurrence and development of cancer; however, the role of circRNA in hypopharyngeal cancer has little been investigated. We performed hypopharyngeal carcinoma circRNA microarray and qRT-PCR verification. The results showed circ_0058106 expression level was significantly upregulated in tumor tissues than in corresponding normal tissues. We found that circ_0058106 upregulation promoted proliferation, migration and invasion of HSCC cells, while knockdown of circ_0058106 inhibited proliferation, migration and invasion of HSCC cells both in vitro and in vivo. Bioinformatics predicted circ_0058106 may interact with miR-185-3p. We verified circ_0058106 directly bound miR-185-3p and downregulated miR-185-3p expression by using dual-luciferase reporter assay and qRT-PCR. Moreover, we proved circ_0058106 promoted HSCC cells tumorigenesis and EMT process by regulating Wnt2b/β-catenin/c-Myc pathway via miR-185-3p. In conclusion, our findings firstly confirmed the carcinogenic effect of circ_0058106 in promoting HSCC cells tumorigenesis, metastasis, invasion and EMT process by regulating Wnt2b/β-catenin/c-Myc pathway through sponging miR-185-3p, indicating that circ_0058106 may be a new therapeutic target and prognostic marker for HSCC.

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.

scholarly journals A Feed-Forward Regulatory Loop between HuR and the Long Noncoding RNA HOTAIR Promotes Head and Neck Squamous Cell Carcinoma Progression and Metastasis

2016 ◽  
Vol 40 (5) ◽  
pp. 1039-1051 ◽  
Author(s):  
Cheng-Zhi Xu ◽  
Chenyan Jiang ◽  
Qingwei Wu ◽  
Liu Liu ◽  
Xiaojun Yan ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Viability ◽  
Cell Carcinoma ◽  
Head And Neck ◽  
Squamous Cell ◽  
Neck Squamous Cell Carcinoma ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Qrt Pcr ◽  
Regulatory Loop

Background/Aims: The lncRNA Homeobox (HOX) transcript antisense RNA (HOTAIR) is overexpressed in numerous cancers. HuR is also overexpressed during tumourigenesis and is abnormally present within the cytoplasm, where it binds to AU-rich elements in the 3′UTRs of target mRNA and post-transcriptionally regulates the expression of its target genes. However, whether HOTAIR is regulated and the mechanisms by which it affects head and neck squamous cell carcinoma (HNSCC) are not well understood. Methods: MTT, cell cycle arrest and apoptotic assays were used to examine the effects of HOTAIR and HuR on cell viability in SCC25 and FaDu cells. Wound healing and transwell invasion analysis were performed to detect the effects of HOTAIR and HuR on cell migration and invasion. The interaction between HuR and HOTAIR was confirmed via qRT-PCR, western blots, luciferase reporter and RIP assays. Finally, qRT-PCR analysis was used to detect the levels of HuR and HOTAIR in HNSCC tumours and adjacent normal tissues. Results: Knockdown of HOTAIR and HuR decreased cell viability, cellular migration and invasion. Moreover, HuR interacted and stabilized HOTAIR stability and thus promoted HOTAIR expression. Notably, HOTAIR acted as a miRNA sponge for HuR. HuR also reinforced HOTAIR sponge activity through miRNA recruitment, thus enhancing HuR expression in turn. Finally, HuR and HOTAIR levels were positively correlated and significantly up-regulated in tumours samples. Conclusion: We demonstrated the existence of a regulatory loop in which the expression of HOTAIR and HuR is reciprocally and temporally regulated during the metastasis and progression of HNSCC.

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 SHISA3Promoter Methylation Is a Potential Diagnostic and Prognostic Biomarker for Laryngeal Squamous Cell Carcinoma

2017 ◽  
Vol 2017 ◽  
pp. 1-8 ◽  
Author(s):  
Zhisen Shen ◽  
Chongchang Zhou ◽  
Jinyun Li ◽  
Dong Ye ◽  
Hongxia Deng ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Promoter Methylation ◽  
Laryngeal Squamous Cell Carcinoma ◽  
Prognostic Biomarker ◽  
Promoter Hypermethylation ◽  
Luciferase Reporter ◽  
Regulatory Function ◽  
Qrt Pcr

The purpose of this study was to evaluate the contribution ofSHISA3promoter methylation to laryngeal squamous cell carcinoma (LSCC).SHISA3promoter methylation status and expression were determined using methylation-specific polymerase chain reaction (MSP) and quantitative real-time PCR (qRT-PCR) in 93 paired LSCC and adjacent normal tissues, respectively. Furthermore, the regulatory function of theSHISA3promoter fragment was analyzed using a luciferase reporter assay. The results reveal that there is a significant increase inSHISA3methylation in LSCC tissues compared with corresponding nontumor tissuesP=4.58E-12. The qRT-PCR results show a significant association betweenSHISA3methylation and expression in LSCCP=1.67E-03. In addition, the area under the receiver operating characteristic curve was 0.91. Consequently, a log-rank test and multivariate Cox analysis suggest thatSHISA3promoter hypermethylation is a predictor of poor overall survival for LSCC (log-rankP= 0.024; HR = 2.71; 95% CI = 1.024–7.177;P= 0.047). The results indicate thatSHISA3promoter hypermethylation might increase the risk of LSCC through regulation of gene expression and is a potential diagnostic and prognostic biomarker for LSCC.

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 Long Non-Coding RNA CCAT2 Promotes the Development of Esophageal Squamous Cell Carcinoma by Inhibiting miR-200b to Upregulate the IGF2BP2/TK1 Axis

2021 ◽  
Vol 11 ◽  
Author(s):  
Xiaodan Wu ◽  
Yihui Fan ◽  
Yupeng Liu ◽  
Biao Shen ◽  
Haimin Lu ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Clinical Samples ◽  
Non Coding Rna

Long non-coding RNAs (lncRNAs) have been shown to play important roles in human cancers, including esophageal squamous cell carcinoma (ESCC). In the current study, we identified CCAT2 as a relevant lncRNA and investigated its role in the progression of ESCC. RT-qPCR was adopted to detect CCAT2 expression in collected clinical samples, ESCC cell lines, and a normal cell line. We tested the correlation between CCAT2 expression and the prognosis of ESCC. RT-qPCR or immunoblotting was adopted to detect the expression of relevant factors in ESCC tissues or cells. Cell proliferation, apoptosis, migration, and invasion were examined by colony formation assay, flow cytometry, scratch assay, and Transwell assay, respectively, while subcutaneous tumorigenesis in nude mice was adopted to examine the role of CCAT2 in tumorigenesis of ESCC cells in vivo. Bioinformatics analysis, dual luciferase reporter assay, and RIP were conducted for the target relationship profiling. Me-RIP was adopted to detect m6A modification level of TK1 in ESCC tissues or cells. Upregulated CCAT2, IGF2BP2, and TK1 expression and inhibited miR-200b expression were observed in ESCC cells and tissues. CCAT2 bound to miR-200b and reduced its expression, leading to upregulated IGF2BP2 expression. IGF2BP2 improved TK1 mRNA stability to enhance its expression by recognizing its m6A modification. CCAT2 promoted the migration and invasion of ESCC cells in vitro, and tumorigenesis in vivo by upregulating TK1 expression, while overexpression of miR-200b reversed these effects of CCAT2. Overall, this study suggests that CCAT2 competitively binds to miR-200b to alleviate its inhibitory effects on IGF2BP2 expression, resulting in elevated TK1 expression, and an ensuing promotion of the development of ESCC.

Circ_DLG1 facilitates esophageal squamous cell carcinoma progression by mediating miR-338-3p/MAP3K9 axis via activating MAPK/ERK pathway

2020 ◽  
Author(s):  
Yixuan Yang ◽  
Bing Zhu ◽  
Zhaofeng Ning ◽  
Xiaodong Wang ◽  
Zhaoxia Li ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Mitogen Activated Protein Kinase ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Erk Pathway

Abstract Background: Esophageal squamous cell carcinoma (ESCC) is an aggressive malignancy with a high incidence and poor prognosis. The document of circular RNAs (circRNAs) is frequently associated with cancer development. This study intended to explore the functional mechanism of circ_DLG1 in ESCC.Methods: The expression of circ_DLG1, miR-338-3p and Mitogen-Activated Protein Kinase Kinase Kinase 9 (MAP3K9) was measured by quantitative real-time polymerase chain reaction (qRT-PCR). Cell cycle, proliferation, migration and invasion were performed for functional analysis using flow cytometry, 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) and transwell assay, respectively. The protein levels of MAP3K9, p38, phosphor p38 (p-p38), ERK1/2, phosphor ERK1/2 (p-ERK1/2) were detected by western blot. Bioinformatics tool for target prediction used the online tool starBase. Dual-luciferase reporter assay was performed to verify the target relationship. The animal experiments were performed to ascertain the role of circ_DLG1 in vivo.Results: The expression of circ_DLG1 was elevated in ESCC tissues, plasma and cells. Circ_DLG1 knockdown inhibited cell cycle, proliferation, migration and invasion. MAP3K9 was highly expressed in ESCC tissues and cells, and its overexpression rescued the effects of circ_DLG1 knockdown. MiR-338-3p was a link between circ_DLG1 and MAP3K9, and circ_DLG1 regulated the expression of MAP3K9 by targeting miR-338-3p. The MAPK/ERK pathway was involved in the circ_DLG1/miR-338-3p/MAP3K9 regulatory axis. Circ_DLG1 knockdown blocked the tumor growth in vivo by regulating miR-338-3p and MAP3K9.Conclusion: Circ_DLG1 contributed to the malignant progression of ESCC by mediating the miR-338-3p/MAP3K9 axis via activating the MAPK/ERK signaling pathway. This paper provided a novel action mode of circ_DLG1 in ESCC.

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.

PS02.053: DUAL-STRANDS OF MIR-150-DUPLEX (MIR-150–5P AND MIR-150–3P) ACTED AS ANTI-TUMOR MIRNAS THROUGH TARGETING SPOCK1 IN ESOPHAGEAL SQUAMOUS CELL CARCINOMA

2018 ◽  
Vol 31 (Supplement_1) ◽  
pp. 135-135
Author(s):  
Yusaku Osako ◽  
Naohiko Seki ◽  
Tetsuya Idichi ◽  
Yoshiaki Kita ◽  
Itaru Omoto ◽  
...  
Keyword(s):  
Gene Expression ◽  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Cancer Cell ◽  
Squamous Cell ◽  
Fine Tuning ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Passenger Strand

Abstract Background MicroRNAs (miRNAs) belong to a group of small non-coding RNA molecules that act as pivotal agents responsible for fine-tuning RNA expression in a sequence-dependent manner. A large number of studies showed that dysregulated miRNAs are deeply involved in the development of cancer cells, as well as their metastasis and drug resistance. Based on our original miRNA expression signatures by RNA-sequencing revealed that both strands of miR-150–5p (the guide strand) and miR-150–3p (the passenger strand) was downregulated in several cancers. The general concept of miRNA biogenesis posits that the passenger strand of miRNA (the minor strand or miRNA*) derived from duplex miRNA is degraded and does not regulate gene expression. Here, we aimed that to investigate functional significance of these miRNAs in esophageal squamous cell carcinoma (ESCC). Methods Cancer cell proliferation, migration and invasion abilities were performed by using mature miRNAs or siRNAs. Genome-wide gene expression analyses and in silico analyses were applied to identify miRNA target genes in ESCC cells. Results Expression levels of miR-150–5p and miR-150–3p were significantly reduced in ESCC clinical specimens and cell lines. Cancer cell aggressiveness was inhibited by ectopic expression of these miRNAs. A total of 12 genes were identified as oncogenic targets by both miR-150–5p and miR-150–3p in ESCC cells. SPOCK1 (SPARC/osteonectin, cwcv and kazal-like domains proteoglycan 1) was directly regulated by both miR-150–5p and miR-150–3p by luciferase reporter assay. Overexpression of SPOCK1 was detected in ESCC specimens and knockdown of SPOCK1 by siRNA significantly inhibited cancer cell migration and invasion abilities. Conclusion Both strands of miR-150-duplex (miR-150–5p and miR-150–3p) acted as anti-tumor miRNAs in ESCC. Overexpression of SPOCK1 was enhanced cancer cell aggressiveness. Involvement of passenger strand of miRNA in cancer pathogenesis is novel concept in cancer research. We suggest that identification of novel function of passenger strands of miRNAs and the RNA networks they regulate might enhance our understanding of the molecular pathogenesis of ESCC. Disclosure All authors have declared no conflicts of interest.

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.

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