MiR-454 Prompts Cell Proliferation of Human Colorectal Cancer Cells by Repressing CYLD Expression

Liu, Hongliang; Hu, Aiping; Li, Senlin; Xie, Jia-Ping; Qiang, Ma; Liu, Jiyong

doi:10.7314/apjcp.2015.16.6.2397

Cited by 36 publications

(34 citation statements)

References 24 publications

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“…miR-454 was also identified to be downregulated in glioblastoma tissues (23). However, in colorectal cancer and uveal melanoma, miR-454 was significantly upregulated in tumor tissues and cell lines (24,25). Yu et al (26) revealed that miR-454 expression was increased in hepatocellular carcinoma tissues and cell lines.…”

Section: Discussionmentioning

confidence: 99%

“…The detailed functions of miR-454 in human cancer have been sufficiently investigated. Liang et al (24) demonstrated that miR-454 overexpression enhanced the proliferation and anchorage-independent growth of colorectal cancer cells, whereas miR-454 under expression decreased this effect. In osteosarcoma, ectopic expression of miR-454 suppressed cell proliferation and invasion (22).…”

Section: Discussionmentioning

confidence: 99%

“…The identification of miR-454 target genes is essential for understanding its molecular mechanism in carcinogenesis and tumor development, and for the development of novel targeted therapies. Multiple target genes have been validated, including CYLD lysine 63 deubiquitinase (24) in colorectal cancer, MET proto-oncogene receptor tyrosine kinase (22) in osteosarcoma, chromodomain helicase DNA binding protein 5 (26) in hepatocellular carcinoma, phosphatase and tensin homolog in uveal melanoma (25) and pyruvate dehydrogenase kinase 1 (23) in glioblastoma. In the present study, ZEB1 was successfully identified to be a novel direct target gene of miR-454.…”

Section: Discussionmentioning

confidence: 99%

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MicroRNA-454 inhibits tumor cell proliferation, migration and invasion by downregulating zinc finger E-box-binding homeobox 1 in gastric cancer

Song

Wang

et al. 2017

Molecular Medicine Reports

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Gastric cancer is the fourth most common malignancy and the third leading cause of cancer‑associated mortality globally. Accumulating studies have identified the involvement of microRNAs in the initiation and progression of gastric cancer. This study was aimed to investigate the expression, functional roles of microRNA‑454 (miR‑454) and its direct target gene in gastric cancer. According to the results, the expression level of miR‑454 was demonstrated to be reduced in gastric cancer tissues and cell lines compared with corresponding distant non‑tumor gastric tissues and human immortalized gastric epithelial, respectively. miR‑454 mimic transfection led to inhibition of gastric cancer cells proliferation, migration and invasion in vitro. Bioinformatic analysis predicated that zinc finger E‑box‑binding homeobox 1 (ZEB1) is a potential target gene of miR‑454. Luciferase reporter assays revealed that miR‑454 directly targeted the 3'UTR of ZEB1. miR‑454 overexpression significantly decreased the ZEB1 mRNA and protein expression levels. ZEB1 knockdown could mimic the tumor suppressive roles induced by miR‑454 overexpression on gastric cancer cell proliferation, migration and invasion. In conclusion, the present study suggested that miR‑454 under expression may be involved in gastric cancer initiation and progression, by promoting proliferation, migration and invasion by directly targeting ZEB1. miR‑454/ZEB1‑based targeted therapy may be a potential strategy for the treatment of gastric cancer.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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MicroRNA-454 inhibits tumor cell proliferation, migration and invasion by downregulating zinc finger E-box-binding homeobox 1 in gastric cancer

Song

Wang

et al. 2017

Molecular Medicine Reports

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“…Previous studies have reported this miR to be downregulated in esophageal cancer [43] and upregulated in colorectal cancer and breast cancer. [44,45] miR-454 has been reported to function as an oncogenic miR by targeting PTEN. Patients with TNBC tumors that lose PTEN expression have poorer survival, as PTEN negatively regulates the PI3K-AKT signaling pathway.…”

Section: Discussionmentioning

confidence: 99%

MicroRNAs in the prognosis of triple-negative breast cancer

Mao

Shi

et al. 2017

Medicine

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Background:Triple-negative breast cancer (TNBC) is a heterogeneous group of tumors characterized by their aggressive nature and poor associated survival. MicroRNAs (miRs) have been found to play an important role in the occurrence and development of human cancers, but their role in the prognosis of TNBC patients remains unclear. We performed a meta-analysis to explore the prognostic value of miRs in TNBC.Methods:We systematically searched the PubMed, Embase, and Web of Science databases to identify eligible studies. A meta-analysis was performed to estimate the pooled hazard ratios (HRs) and their corresponding 95% confidence intervals (CIs) for the associations between levels of miR expression (predictive factors) and overall survival (OS) and disease-free survival (DFS) (outcomes) in patients with TNBC.Results:After performing the literature search and review, 21 relevant studies including 2510 subjects were identified. Six miRs (miR-155, miR-21, miR-27a/b, miR-374a/b, miR-210, and miR-454) were assessed in the meta-analysis. Decreased expression of miR-155 was associated with reduced OS (adjusted HR = 0.58, 95% CI: 0.34–0.99; crude HR = 0.67, 95% CI: 0.58–0.79). High miR-21 expression was also predictive of reduced OS (crude HR = 2.50, 95% CI: 1.56–4.01). We found that elevated levels of miR-27a/b, miR-210, and miR-454 expression were associated with shorter OS, while the levels of miR-454 and miR-374a/b expression were associated with DFS.Conclusions:Specific miRs could serve as potential prognostic biomarkers in TNBC. Due to the limited research available, the clinical application of these findings has yet to be verified.

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“…Currently, miR-454 has been discovered to promote tumor progression in multiple organs. 15,16 For example, Zhu et al found that miR-454 was overexpressed in NSCLC samples and closely correlated with lymph node metastasis, advanced TNM stage, and shorter overall survival, 17 study of Sun et al showed that miR-454 functioned as an oncogene in uveal melanoma by regulating PTEN, 15 extensive research has shown that miR-454 strengthened the proliferation, invasion, and epithelial mesenchymal transformation of hepatocellular carcinoma cells, 18 and data from Liang et al 19 and Liu et al 16 demonstrated that miR-454 regulated colon cancer cell proliferation through regulating different signaling pathways. Based on the above research, we understood the importance of miR-454 in tumorigenicity, while the function of miR-454 on OSCC was still unknown.…”

mentioning

confidence: 99%

miR‐454 performs tumor‐promoting effects in oral squamous cell carcinoma via reducing NR3C2

Guo

Wang

et al. 2020

J Oral Pathology Medicine

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Background Aberrant miRNAs expression regulates the occurrence and progression of a variety of cancers, including oral squamous cell carcinoma (OSCC). This study aims to illustrate the potential effects of miR‐454/nuclear receptor subfamily 3 group C member 2 (NR3C2) on the biological behaviors of OSCC cells. Methods GEO database was applied to detect and analyze the expression of miR‐545 and NR3C2 in OSCC tissues. Two OSCC cell lines including CAL27 and Tca‐83 were utilized to determine the function of miR‐454/NR3C2 on OSCC cells biological behaviors. miR‐454 and NR3C2 expressions were regulated by miR‐454 mimic/inhibitor and pcDNA3.1‐NR3C2/si‐NR3C2, respectively. Cells biological behaviors were evaluated by cell proliferation, colony formation, and transwell assays. Results The data collected from GEO database indicated that miR‐454 expression was upregulated in OSCC tissues; however, the expression of NR3C2 assumed a downward trend. In vitro experiments, the expression trend of miR‐454 in OSCC cell lines was consistent with that of the trend in tissues, and the OSCC cells growth and movement abilities significantly decreased after miR‐454 depletion. Through co‐transfection experiments, we explored that the abilities of OSCC cell proliferation, colony formation, invasion, and migration obviously reduced after miR‐454 depletion, but these phenomena were mitigated to some extent after NR3C2 silencing. Conclusion The study illustrates that miR‐454 acts as an active regulator to facilitate OSCC cells growth, colony formation, invasion, and migration by targeting NR3C2, which may afford a novel perspective and possibility for the targeted treatment of OSCC.

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MiR-454 Prompts Cell Proliferation of Human Colorectal Cancer Cells by Repressing CYLD Expression

Cited by 36 publications

References 24 publications

MicroRNA-454 inhibits tumor cell proliferation, migration and invasion by downregulating zinc finger E-box-binding homeobox 1 in gastric cancer

MicroRNA-454 inhibits tumor cell proliferation, migration and invasion by downregulating zinc finger E-box-binding homeobox 1 in gastric cancer

MicroRNAs in the prognosis of triple-negative breast cancer

miR‐454 performs tumor‐promoting effects in oral squamous cell carcinoma via reducing NR3C2

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