miR-205 promotes proliferation and invasion of laryngeal squamous cell carcinoma by suppressing CDK2AP1 expression

Zhong, Gang; Xiong, Xingao

doi:10.1186/s40659-015-0052-5

Cited by 34 publications

(25 citation statements)

References 42 publications

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“…Previous studies have demonstrated that miR-205 functions as an oncogene in numerous types of human cancer (20)(21)(22). For example, in laryngeal squamous cell carcinoma, miR-205 was upregulated and enhanced cell growth and invasion via negative regulation of CDK2AP1 expression level (20). Expression levels of miR-205 were reported to be increased in endometrial cancer tissues (21).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‑205 is downregulated in hepatocellular carcinoma and inhibits cell growth and metastasis via directly targeting vascular endothelial growth factor A

et al. 2018

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MicroRNAs (miRs) are an emerging class of non-coding, endogenous and small RNA molecules that serve important functions in tumorigenesis and development. The present study investigated the expression, functions and molecular mechanism underlying miR-205 in hepatocellular carcinoma. miR-205 was downregulated in hepatocellular carcinoma tissues and cell lines. Ectopic miR-205 expression suppressed hepatocellular carcinoma cell proliferation, migration and invasion . In addition, vascular endothelial growth factor A (VEGFA) was identified as a functional downstream target of miR-205 in hepatocellular carcinoma. Furthermore, knockdown of VEGFA revealed the same functions with miR-205 overexpression in hepatocellular carcinoma cells. These results provided evidence that miR-205 served important functions in the inhibition of hepatocellular carcinoma cells growth and metastasis via directly targeting VEGFA, which indicated that miR-205 may have therapeutic value for hepatocellular carcinoma.

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Section: Discussionmentioning

confidence: 99%

MicroRNA‑205 is downregulated in hepatocellular carcinoma and inhibits cell growth and metastasis via directly targeting vascular endothelial growth factor A

et al. 2018

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“…A number of target genes of miR-205 have been previously identified, including zinc finger E-box binding homeobox 1 (27) in gastric cancer, tumor protein p53 inducible nuclear protein 1 in prostate cancer (31), transforming growth factor-α in osteosarcoma (20), cyclic AMP responsive element binding protein 1 in colorectal cancer (32), cyclin dependent kinase 1 associated protein 1 in laryngeal squamous cell carcinoma (23) and angiomotin in breast cancer (30). However, no target of miR-205 has been identified in glioma.…”

Section: Discussionmentioning

confidence: 99%

microRNA-205 acts as a tumor suppressor and directly targets YAP1 in glioma

Zhang

2017

Molecular Medicine Reports

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Glioma is the most common form of primary malignant tumor that occurs in the central nervous system. The underlying molecular mechanism of the carcinogenesis and progression of glioma remains to be elucidated. It is well‑established that microRNAs (miRs) are associated with the regulation of glioma initiation and progression, and may represent a novel effective therapeutic strategy for the treatment of glioma. In the present study, the expression, roles and molecular mechanisms of miR‑205 in glioma were investigated. The expression levels of miR‑205 in glioma tissues, normal brain tissues, human glioma and normal HEB glial cell lines were determined using reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR). To explore the functional roles of miR‑205 in glioma cells, a Cell Counting kit 8 assay, and Transwell migration and invasion assays were employed. The molecular mechanisms underlying the roles of miR‑205 in glioma cells were investigated using bioinformatics analysis, a luciferase reporter assay, RT‑qPCR and western blot analysis. The results of the present study demonstrated that miR‑205 expression was markedly low in glioma tissues and cell lines compared with normal brain tissue and a glial cell line. Upregulation of miR‑205 in vitro decreased cell viability, migration and invasion in glioma. Further investigation of the potential molecular mechanism demonstrated that the tumor suppressive functions of miR‑205 in regulating the proliferation, migration and invasion of glioma cells were mediated by a direct target gene, yes associated protein 1 (YAP1). The results of the present study suggested that miR‑205 inhibited glioma growth and metastasis by directly targeting YAP1, and that miR‑205 should be investigated as a novel therapeutic target for anti‑cancer treatment.

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“…Overexpression of miR-613 reduces LSCC cell proliferation, invasion, and blocks G1/S phase transition by targeting the PDK1 gene [13]. Furthermore, miR-1297, miR-143-3p, miR-503 and miR-205 also promote LSCC cell progression [14][15][16][17]. Recent studies have confirmed that miR-17-5p plays critical roles in tumor progression, such as pancreatic cancer, breast cancer, hepatocellular carcinoma, gastric cancer and prostate cancer [18][19][20][21][22].…”

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confidence: 97%

Silencing of miR-17-5p suppresses cell proliferation and promotes cell apoptosis by directly targeting PIK3R1 in laryngeal squamous cell carcinoma

et al. 2020

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Background: Increasing evidence has suggested that microRNAs (miRNAs) act as key post-transcriptional regulators in tumor progression. Previous studies have confirmed that miR-17-5p functions as an oncogene in multiple cancers and contributes to tumor progression. However, the role and biological functions of miR-17-5p in the development of laryngeal squamous cell carcinoma (LSCC) still remain unknown.Methods: qRT-PCR was used to detect miRNA and mRNA expression levels in LSCC tissues and cell lines. CCK-8 assay was used to measure cell viability and flow cytometry was performed to evaluate cell apoptosis. Western blot analysis was used to detect the protein levels of BAX, BCL-2, cleaved Caspase-3, PIK3R1 and AKT. Luciferase reporter assay was used to detect the effect of miR-17-5p on PIK3R1 expression. Xenograft animal model was used to test the effect of miR-17-5p on LSCC cell in vivo. Results:In the present study, we found that miR-17-5p expression level was upregulated in LSCC tissues and cell lines. Depletion of miR-17-5p in LSCC cells significantly reduced cell proliferation and promoted cell apoptosis in vitro and in vivo. Mechanically, knockdown of miR-17-5p in LSCC cells inhibited BCL-2 expression while enhanced BAX and cleaved Caspase-3 protein expression. Moreover, depletion of miR-17-5p in LSCC cells suppressed AKT phosphorylation but did not influence PTEN expression. Importantly, miR-17-5p positively regulated PIK3R1 expression by directly binding to its 3′-untranslated region (UTR). Additionally, PIK3R1, which expression was downregulated in LSCC tissues and cell lines, was involved in LSCC cell survival by modulating the activation of AKT signal pathway. Dysregulation of miR-17-5p/PIK3R1 axis was participated in LSCC cell proliferation and apoptosis by inhibiting the activation of the PI3K/AKT signaling pathway. Conclusions:In conclusion, our study indicates that the miR-17-5p/PIK3R1 axis plays an essential role in the development of LSCC and provides a potential therapeutic target for LSCC treatment. BackgroundLaryngeal squamous cell carcinoma (LSCC) is the most common head and neck malignancy accounting for more than 95% of head and neck squamous cell carcinoma (HNSCC), with 177,422 new cases and 94,771

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miR-205 promotes proliferation and invasion of laryngeal squamous cell carcinoma by suppressing CDK2AP1 expression

Cited by 34 publications

References 42 publications

MicroRNA‑205 is downregulated in hepatocellular carcinoma and inhibits cell growth and metastasis via directly targeting vascular endothelial growth factor A

MicroRNA‑205 is downregulated in hepatocellular carcinoma and inhibits cell growth and metastasis via directly targeting vascular endothelial growth factor A

microRNA-205 acts as a tumor suppressor and directly targets YAP1 in glioma

Silencing of miR-17-5p suppresses cell proliferation and promotes cell apoptosis by directly targeting PIK3R1 in laryngeal squamous cell carcinoma

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