Overexpression of A disintegrin and metalloprotease 10 promotes tumor proliferation, migration and poor prognosis in hypopharyngeal squamous cell carcinoma

Ding, Chuanjin; Zhang, Qicheng; Chen, Yan; Zhang, Xiaobo; Wu, Pei Hsun; Zhang, Zhenxin

doi:10.3892/or.2017.5761

Cited by 3 publications

(3 citation statements)

References 36 publications

(49 reference statements)

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“…Revealing studies have suggested the potential role of ADAM10 in cell migration and metastasis in various cancers including HCC. In hypopharyngeal squamous cell carcinoma (HSCC), high expression of ADAM10 was suggested to increase epithelial-mesenchymal transition (EMT) regulation, and promote tumor cell migration and infiltration 23 . In human esophageal squamous cell carcinoma (ESCC), active ADAM10 was suggested to promote the carcinogenesis, invasion, metastasis, and proliferation of ESCC and control invasion and metastasis through shedding E-cadherin activity 24 .…”

Section: Discussionmentioning

confidence: 99%

Impact of ADAM10 gene polymorphisms on hepatocellular carcinoma development and clinical characteristics

Shiu¹,

Hsieh²,

Chiou³

et al. 2018

Int. J. Med. Sci.

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A disintegrin and metalloprotease (ADAM) family proteins are type-I transmembrane glycoproteins with multiple functions in cell adhesion, migration, proteolysis and signaling. ADAM10 is a member of the ADAM family reportedly involved in cancer progression and has been shown to be overexpressed in hepatocellular carcinoma (HCC) tissues and significantly associated with tumor progression and shortened survival. This study investigated ADAM10's single nucleotide polymorphisms (SNPs) and their association to HCC development and regulation. Real-time polymerase chain reaction was used to analyze five SNPs of ADAM10 in 333 patients with HCC and 1196 controls without cancer. The results indicated that of the 333 patients with HCC, those who carried ADAM10 rs514049 (AC + CC) variants had a higher risk of developing lymph node metastasis (odds ratio [OR] = 5.087, p = 0.027), and those who carried ADAM10 rs653765 (GA + AA) variants had a higher risk of developing distant metastasis (OR = 3.346, p = 0.020) and higher levels of α-fetoprotein. In conclusion, our study demonstrated that the SNPs of ADAM10 are involved in HCC progression. ADAM10 SNPs may be used as therapeutic targets to evaluate poor prognoses for HCC.

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Section: Discussionmentioning

confidence: 99%

Impact of ADAM10 gene polymorphisms on hepatocellular carcinoma development and clinical characteristics

Shiu¹,

Hsieh²,

Chiou³

et al. 2018

Int. J. Med. Sci.

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show abstract

“…A further study illustrated that miR-489-3p directly bound to ADAM10 3'UTR, suggesting that miR-489-3p might block the function of ADAM10. ADAM10 overexpression was reported to trigger tumor cell proliferation and migration and result in a poor prognosis of HSCC [33]. ADAM10 was also identified to be a target of miR-140-5p, and ADAM10 knockdown suppressed HSCC cell proliferation, migration, and invasion [34].…”

Section: Discussionmentioning

confidence: 99%

Metformin Inhibits the Development of Hypopharyngeal Squamous Cell Carcinoma through Circ_0003214-Mediated MiR-489-3p-ADAM10 Pathway

Chen

et al. 2021

Journal of Oncology

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Purpose. This study aims to explore the function of metformin in hypopharyngeal squamous cell carcinoma (HSCC) and the underlying mechanism. Methods. Cell viability, colony formation, cell apoptosis, and cell cycle were investigated using cell counting kit-8 assay, colony formation, and flow cytometry assay. Gene expression was detected by quantitative real-time polymerase chain reaction and western blot. The target relationship was validated by dual-luciferase reporter assay or RNA immunoprecipitation assay. An animal study was implemented to clarify the effect of metformin in vivo. Results. Metformin suppressed HSCC cell viability and colony formation ability and induced cell cycle arrest and apoptosis, and circ_0003214 overexpression weakened these effects. Circ_0003214 regulated A disintegrin and metalloproteinase domain-containing protein 10 (ADAM10) expression via targeting miR-489-3p. Besides, miR-489-3p restoration reversed the role of circ_0003214, and ADAM10 knockdown reversed miR-489-3p inhibition-mediated effect. Moreover, metformin blocked tumor growth via the circ_0003214-miR-489-3p-ADAM10 axis in vivo. Conclusion. Metformin inhibits HSCC progression through the circ_0003214/miR-489-3p/ADAM10 pathway.

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“…Cell proliferation was analyzed by a CCK-8 kit (KGA317, Beyotime Institute of Biotechnology) [21]. Briefly, cells (4 × 10 3 per well) were seeded into 96-well plates and each group contained five replicates.…”

Section: Cell Counting Kit-8 (Cck-8) Assaymentioning

confidence: 99%

ADAM10 promotes cell growth, migration, and invasion in osteosarcoma via regulating E-cadherin/β-catenin signaling pathway and is regulated by miR-122-5p

Yuan

Chen

et al. 2020

Cancer Cell Int

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Background: Osteosarcoma is a malignant bone tumor. Increasing evidences have revealed that a disintegrin and metalloproteinase 10 (ADAM10) is implicated in tumor development. The main purpose of this study is to explore the effects of ADAM10 on osteosarcoma cell functions and the underlying molecular mechanisms. Methods: Western blot and quantitative real-time PCR were performed to detect the expression of ADAM10 in one osteoblast (hFOB 1.19) and six osteosarcoma cells (Saos-2, SW1353, HOS, U-2OS, MG63, and 143B). The biological functions of ADAM10 in osteosarcoma cells were measured by cell counting kit-8 assay, flow cytometry, wound healing assay, and transwell assay. The interaction between miR-122-5p and ADAM10 was validated using dual-luciferase reporter assay. The effect of ADAM10 on the tumorigenicity of osteosarcoma cells was evaluated in a nude mice model in vivo. Results: We found that the expression of ADAM10 was relatively high in osteosarcoma cells compared with that in osteoblast. ADAM10 promoted osteosarcoma cell growth, migration, and invasion. Mechanism studies showed that knockdown of ADAM10 inactivated E-cadherin/β-catenin signaling pathway, as evidenced by increased the level of E-cadherin, reduced nuclear translocation of β-catenin, and decreased the levels of MMP-9, Cyclin D1, c-Myc, and Survivin. Downregulation of ADAM10 suppressed the tumorigenicity of osteosarcoma cells in vivo. Furthermore, ADAM10 was validated to be a downstream target of microRNA-122-5p (miR-122-5p). MiR-122-5p-induced inhibition of cell proliferation, migration, and invasion was reversed by overexpression of ADAM10 in osteosarcoma cells. Conclusions: Collectively, the key findings of this study are that ADAM10 promotes osteosarcoma cell proliferation, migration, and invasion by regulating E-cadherin/β-catenin signaling pathway, and miR-122-5p can target ADAM10, indicating that miR-122-5p/ADAM10 axis might serve as a therapeutic target of osteosarcoma.

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Overexpression of A disintegrin and metalloprotease 10 promotes tumor proliferation, migration and poor prognosis in hypopharyngeal squamous cell carcinoma

Cited by 3 publications

References 36 publications

Impact of ADAM10 gene polymorphisms on hepatocellular carcinoma development and clinical characteristics

Impact of ADAM10 gene polymorphisms on hepatocellular carcinoma development and clinical characteristics

Metformin Inhibits the Development of Hypopharyngeal Squamous Cell Carcinoma through Circ_0003214-Mediated MiR-489-3p-ADAM10 Pathway

ADAM10 promotes cell growth, migration, and invasion in osteosarcoma via regulating E-cadherin/β-catenin signaling pathway and is regulated by miR-122-5p

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