microRNA-495 promotes bladder cancer cell growth and invasion by targeting phosphatase and tensin homolog

Tan, Mingyue; Mu, Xingyu; Liu, Zhihong; Le, Tao; Wang, Jun; Ge, Jianli; Qiu, Jianxin

doi:10.1016/j.bbrc.2017.01.019

Cited by 37 publications

(33 citation statements)

References 21 publications

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“…In lung cancer, miR-495 is involved in the regulation of cell proliferation, migration, epithelial-mesenchymal transition, chemosensitivity and chemoresistance (40,41,46). However, Tan et al indicated that miR-495 serves as an oncogene in bladder cancer through the regulation of cell proliferation and invasion (18). These conflicting findings suggested that the functional roles of miR-495 in human malignancies may be multifaceted and mainly dependent on involved tissues and their target genes.…”

Section: Discussionmentioning

confidence: 84%

“…For example, miR-495 is upregulated in bladder cancer tissues and cell lines. High miR-495 expression levels are correlated with tumour size, TNM stage and lymph node metastasis of patients with bladder cancer (18). However, miR-495 in medulloblastoma is downregulated in tumour tissues compared with that in normal cerebellum tissues.…”

Section: Discussionmentioning

confidence: 99%

“…The following target miR-495 genes have been identified: HMGN5 (19) in osteosarcoma; GFI1 (35) in medulloblastoma; Glut1 (42), MYB (43) and CDK6 (44) in glioma; FZD4 (36), Akt (45) and mTOR (45) in prostate cancer; SATB1 (37) in renal cell carcinoma; STAT-3 (38) and Bmi-1 (39) in breast cancer; epithelial and endothelial tyrosine kinase (40), MTA3 (41) and ATP7A (46) in lung cancer; and PTEN (18) in bladder cancer. In our study, IGF1R was demonstrated to be a direct functional downstream target of miR-495 in HCC.…”

Section: Discussionmentioning

confidence: 99%

“…Therefore, the expression and molecular mechanisms of miRNAs in human cancers should be further investigated to propose therapeutic targets for anticancer treatments. miR-495, mapped in the 14q32.31 region, is abnormally expressed in multiple types of human cancers, such as upregulated in bladder cancer (18), and downregulated in osteosarcoma (19), melanoma (20), endometrial cancer (21), acute myeloid leukaemia (22). However, the expression level and roles of miR-495 in HCC have yet to be completely elucidated.…”

Section: Introductionmentioning

confidence: 99%

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MicroRNA‑495 suppresses cell proliferation and invasion of hepatocellular carcinoma by directly targeting insulin‑like growth factor receptor‑1

Zhuang

Wang

et al. 2017

Exp Ther Med

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Abstract. Hepatocellular carcinoma (HCC) is the fifth most common malignancy and second-most frequent cause of cancer-associated deaths worldwide. Previously, increasing studies report that microRNAs (miRNAs/miRs) are abnormally expressed in various types of human cancers and may participate in the tumourigenesis and tumour development of HCC. miRNA-based targeted therapy is effective against different molecular targets and may increase the sensitisation of cancer cells to therapy by several folds. Therefore, further validation of potentially important miRNAs involved in HCC initiation and progression may provide valuable insights into the treatment of patients with HCC. miR-495 is abnormally expressed in multiple types of human cancers. However, the expression level and roles of miR-495 in HCC have yet to be completely elucidated. In the present study, miR-495 expression was frequently downregulated in HCC tissues and cell lines, and miR-495 expression levels were significantly correlated with tumour size, tumor-node-metastasis (TNM) stage and lymph node metastasis in patients with HCC. Functional assays revealed that miR-495 overexpression inhibited cell proliferation and invasion in HCC. Insulin-like growth factor receptor-1 (IGF1R) was identified as a direct target gene of miR-495 in HCC. IGF1R was upregulated in HCC tissues and negatively correlated with miR-495 expression level. The upregulation of IGF1R rescued the miR-495-induced tumour-suppressive roles in HCC cell proliferation and invasion, and the restored miR-495 expression inactivated the protein kinase B and extracellular regulated protein kinase signalling pathways in HCC. These results provide novel insights into the molecular mechanism underlying HCC progression, and suggest that miR-495 may be investigated as a novel therapeutic target for patients with this disease.

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Section: Discussionmentioning

confidence: 84%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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MicroRNA‑495 suppresses cell proliferation and invasion of hepatocellular carcinoma by directly targeting insulin‑like growth factor receptor‑1

Zhuang

Wang

et al. 2017

Exp Ther Med

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“…It has been reported that miR-495 suppresses the aggressive behaviors of glioma [11], prostate cancer [12] and esophageal squamous cell carcinoma cells [13]. However, in breast [14], bladder [15] and gastric [16] cancer cells, this miRNA promotes tumor invasion and migration. Importantly, there has been no research focusing on the role of miR-495 in osteosarcoma metastasis.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-495 suppresses osteosarcoma invasion and migration by targeting HSP90AA1

Xiao¹,

Wang²,

Li³

et al. 2018

Oncotarget

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MiR-495 is a tumor-suppressive microRNA that participates in tumor progression in human cancers. However, its expression and biological function in osteosarcoma remains unknown. In this study, we firstly found that miR-495 is markedly downregulated in both osteosarcoma tissues and cell lines. Then we demonstrated that miR-495 suppresses the invasion and metastasis of osteosarcoma cells in vitro through inhibiting epithelial to mesenchymal transition. Function of miR-495 in vivo was also examined in mice xenograft model and we found it significantly inhibiting the lung-metastasis of osteosarcoma cells. We also demonstrated that HSP90AA1 is a direct target of miR-495 using luciferase reporter assay and Western blot analysis. Furthermore, knockdown of HSP90AA1 can restore the increased cell invasion and migration in miR-495-knockdown cells and over expression of HSP90AA1 can neutralize the impaired metastatic ability of miR-495 mimic-treated cells. This metastasis-suppressive role of miR-495 in osteosarcoma is achieved by HSP90AA1-mediated PI3K/Akt/mTOR signaling pathway. Overall, our findings proved for the first time that miR-495 acts as a tumor suppressor in osteosarcoma and inhibits cell migration and invasion by targeting HSP90AA1, thus offering a promising therapeutic target for osteosarcoma treatment.www.impactjournals.com/oncotarget/

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miR‐495 and miR‐5688 are down‐regulated in non‐small cell lung cancer under hypoxia to maintain interleukin‐11 expression

Zhao

Chang

Liu

et al. 2020

Cancer Communications

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Background Hypoxia is a hallmark of cancer and is associated with poor prognosis. However, the molecular mechanism by which hypoxia promotes tumor progression remains unclear. MicroRNAs dysregulation has been shown to play a critical role in the tumor and tumor microenvironment. Here, we investigated the roles of miR‐495 and miR‐5688 in human non‐small cell lung cancer (NSCLC) and their underlying mechanism. Methods The expression levels of miR‐495 and miR‐5688 in human NSCLC tissue specimens were measured by quantitative real‐time polymerase chain reaction (qRT‐PCR). Deferoxamine (DFO) was used to determine whether the regulation of miR‐495 and miR‐5688 under hypoxia was dependent on hypoxia‐inducible factor 1‐alpha (HIF‐1α). Furthermore, the functions of miR‐495 and miR‐5688 in tumor progression were evaluated using colony formation, 3‐(4,5‐dimethylthiazol‐2‐yl)‐5‐(3‐carboxymethoxyphenyl)‐2‐(4‐sulfophenyl)‐2H‐tetrazolium (MTS), wound healing, transwell assays, and xenograft model. Two algorithms, PicTAR and Targetscan, were used to predict the target gene of these two miRNAs, and dual‐luciferase reporter assay was conducted to confirm the target. The unpaired two‐tailed t test, Pearson correlation analysis, and Fisher's exact probability test were performed for statistical analyses. Results Two miRNAs, miR‐495 and miR‐5688, were found to participate in NSCLC progression under hypoxia. They were down‐regulated in NSCLC tissues compared with normal tissues. We determined that hypoxia led to the down‐regulation of miR‐495 and miR‐5688 in NSCLC cells, which was independent of HIF‐1α and cellular metabolic energy. In addition, miR‐495 and miR‐5688 suppressed cell proliferation, migration, and invasion in vitro. The NSCLC xenograft model showed that miR‐495 and miR‐5688 inhibited tumor formation in vivo. Interestingly, we found that miR‐495 and miR‐5688 had the same target, interleukin‐11 (IL‐11). Recombinant human IL‐11 counteracted the effects of miR‐495 and miR‐5688 on NSCLC cells, suggesting that miR‐495 and miR‐5688 executed their tumor suppressive role by repressing IL‐11 expression. Conclusion We found that hypoxia down‐regulated the expression levels of miR‐495 and miR‐5688 in NSCLC to enhance IL‐11 expression and tumor progression, indicating that the miR‐495/miR‐5688/IL‐11 axis may serve as a therapeutic target and potential biomarker for NSCLC.

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microRNA-495 promotes bladder cancer cell growth and invasion by targeting phosphatase and tensin homolog

Cited by 37 publications

References 21 publications

MicroRNA‑495 suppresses cell proliferation and invasion of hepatocellular carcinoma by directly targeting insulin‑like growth factor receptor‑1

MicroRNA‑495 suppresses cell proliferation and invasion of hepatocellular carcinoma by directly targeting insulin‑like growth factor receptor‑1

MicroRNA-495 suppresses osteosarcoma invasion and migration by targeting HSP90AA1

miR‐495 and miR‐5688 are down‐regulated in non‐small cell lung cancer under hypoxia to maintain interleukin‐11 expression

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