miR-375 and miR-205 Regulate the Invasion and Migration of Laryngeal Squamous Cell Carcinoma Synergistically via AKT-Mediated EMT

Wang, Bin; Lv, Kexing; Chen, Weixiong; Zhao, Jing; Luo, Jie; Wu, Jianhui; Li, Zenghong; Qin, Hao; Wong, Thomas K. F.; Yang, Weiqiang; Fu, Qing‐Ling; Lei, Wenbin

doi:10.1155/2016/9652789

Cited by 31 publications

(19 citation statements)

References 34 publications

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“…First of all, the 5-year survival rate of non-small cell lung carcinoma (NSCLC) is only 11%, which means most patients can not get completely cured after their therapy [2]. Second, tumor invasion and metastasis are the major problems in disease progression and therapy failure, which cause immense cases of decease [3]. Thence, a strategy of prevention from tumor metastasis is really essential.…”

Section: Introductionmentioning

confidence: 99%

Long non-coding RNA FGD5-AS1 promotes non-small cell lung cancer cell proliferation through sponging hsa-miR-107 to up-regulate FGFRL1

Fan

Li²,

et al. 2020

Bioscience Reports

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Long non-coding RNA (lncRNA) FYVE, RhoGEF and PH domain containing 5 antisense RNA 1 (FGD5-AS1) has been reported as an oncogene in colorectal cancer, promoting its tumorgenesis. The present paper focused on searching the potential function of FGD5-AS1 in non-small cell lung carcinoma (NSCLC). There are connections between the expression of lncRNA FGD5-AS1 and human NSCLC tumor growth and progression. Also, the relationships between FGD5-AS1, hsa-miR-107 and mRNA fibroblast growth factor receptor like 1 (FGFRL1) are going to test their interaction in NSCLC cell lines, which may cause a series of biological behaviors of NSCLC cells. qRT-PCR analysis was conducted to test the expression of RNAs in different situation. CCK-8 experiment and clone formation assay were performed to assess proliferation of NSCLC cells. Also, connection between FGD5-AS1 and hsa-miR-107 were investigated by luciferase reporter assay and RNA pull-down assay. Rescue experiments were performed to verify the modulating relationship between FGD5-AS1, hsa-miR-107 and FGFRL1. High-level expression of FGD5-AS1 was found in NSCLC. FGD5-AS1 may promote the proliferation of NSCLC cells. Also, the combination between hsa-miR-107, FGD5-AS1 and NSCLC have been proved, which means they can play an interaction function in NSCLC cells. Thence, we concluded that lncRNA FGD5-AS1 promotes non-small cell lung cancer cell proliferation through sponging hsa-miR-107 to up-regulate FGFRL1.

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Section: Introductionmentioning

confidence: 99%

Long non-coding RNA FGD5-AS1 promotes non-small cell lung cancer cell proliferation through sponging hsa-miR-107 to up-regulate FGFRL1

Fan

Li²,

et al. 2020

Bioscience Reports

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“…Therefore, investigating molecular biological markers, in order to analyze the invasion and migration of LSCC, is vital for improving the treatment of local invasion and cervical lymph node metastasis in patients with LSCC ( 10 , 11 ). Notably, microRNA (miRNA), such as miRNA-1 and miRNA-205, has been reported to be associated with the invasion and migration of LSCC, which contributed to the understanding of the molecular mechanism underlying the invasion and migration of LSCC ( 12 – 14 ).…”

Section: Introductionmentioning

confidence: 99%

MicroRNA‑153 suppresses human laryngeal squamous cell carcinoma migration and invasion by targeting the SNAI1 gene

Zhang

2018

Oncol Lett

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Human laryngeal squamous cell carcinoma (LSCC) is a malignant cancer type. Epithelial-mesenchymal transition marker Snail family transcriptional repressor 1 (SNAI1) is associated with the occurrence, development, invasion and metastasis of numerous tumor types, such as lung, liver and ovarian cancer. Previous studies have indicated that microRNA-153 (miR-153) may serve as a novel tumor suppressor, which is involved in tumor metastasis; however, the role and clinical significance of miR-153 in LSCC are not fully understood. The aim of the present study was to determine the role of miR-153 in the growth and aggressiveness of LSCC cells. Bioinformatics prediction method, western blot analysis, Matrigel invasion assay and immunofluorescence were used to analyze whether SNAI1 can be regulated and controlled by miR-153 in LSCC cells. An inverse association between miR-153 and SNAI1 was observed in LSCC tissues. It was demonstrated that SNAI1 is a direct target of miR-153 in LSCC. In addition, the results indicated that miR-153 knockdown inhibited PCI-13 cell migration and invasion by targeting SNAI1, which may be a potential marker that can reflect the degree of malignancy in patients with LSCC. Furthermore, miR-153 knockdown decreased Twist family BHLH transcription factor 1 and metastasis-associated 1 family member 3 expression in LSCC cells. In conclusion, these data indicated that miR-153 regulates LSCC migration via the targeting of SNAI1 gene, which may be a potential predictor for patients with LSCC.

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“…A number of studies have demonstrated that ERK1/2 serves arole in the process of EMT in a number of tumors ( 55 – 57 ). Another previous study demonstrated that miR-205 regulates invasion and migration of laryngeal squamous cell carcinoma by AKT-mediated EMT ( 58 ). In the present study, UTMD-mediated miR-205 transfection upregulated the expression of E-cadherin and downregulated MMP-9 expression, suggesting that miR-205 may inhibit EMT in PC-3 cells.…”

Section: Discussionmentioning

confidence: 96%

Ultrasound‑targeted microbubble destruction‑mediated miR‑205 enhances cisplatin cytotoxicity in prostate cancer cells

Qin

Xie

2018

Mol Med Report

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MicroRNAs (miRNAs) are non-coding ~20 nucleotides long sequences that function in the initiation and development of a number of cancers. Ultrasound-targeted microbubble destruction (UTMD) is an effective method for microRNA delivery. The aim of the present study was to investigate the potential roles of UTMD-mediated miRNA (miR)-205 delivery in the development of prostate cancer (PCa). In the present study, miR-205 expression was examined by reverse transcription-quantitative polymerase chain reaction assay. miR-205 mimics were transfected into PC-3 cells using the UTMD method, and the PC-3 cells were also treated with cisplatin. Cell proliferation, apoptosis, migration and invasion abilities were detected using Cell Counting kit-8, flow cytometry, wound healing and Transwell assays, respectively. In addition, the protein expression levels of caspase-9, cleaved-caspase 9, cytochrome c (cytoc), epithelial (E)-cadherin, matrix metalloproteinase-9 (MMP-9), phosphorylated (p)-extracellular signal-regulated kinase (ERK) and ERK were measured by western blot analysis. The results of the present study demonstrated that miR-205 expression was low in human PCa cell lines compared with healthy cells and that UTMD-mediated miR-205 delivery inhibited PCa cell proliferation, migration and invasion, and promoted apoptosis modulated by cisplatin compared with UTMD-mediated miR-negative control group and miR-205-treated group. Furthermore, it was demonstrated that UTMD-mediated miR-205 transfection increased the expression of caspase-9, cleaved-caspase 9, cytochrome c and E-cadherin, and decreased the expression of MMP-9 and p-ERK. Therefore, UTMD-mediated miR-205 delivery may be a promising method for the treatment of PCa.

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miR-375 and miR-205 Regulate the Invasion and Migration of Laryngeal Squamous Cell Carcinoma Synergistically via AKT-Mediated EMT

Cited by 31 publications

References 34 publications

Long non-coding RNA FGD5-AS1 promotes non-small cell lung cancer cell proliferation through sponging hsa-miR-107 to up-regulate FGFRL1

Long non-coding RNA FGD5-AS1 promotes non-small cell lung cancer cell proliferation through sponging hsa-miR-107 to up-regulate FGFRL1

MicroRNA‑153 suppresses human laryngeal squamous cell carcinoma migration and invasion by targeting the SNAI1 gene

Ultrasound‑targeted microbubble destruction‑mediated miR‑205 enhances cisplatin cytotoxicity in prostate cancer cells

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