Hsa-miR-495 acts as a tumor suppressor gene in glioma via the negative regulation of MYB

Zhang, Benping; Yuan, Fei; Liu, Jie; Yang, Li; Zhou, Fucheng; Liu, Xuanxi; Zhou, Hao; Li, Qingsong; Zheng, Yongri; Wang, Weizhi

doi:10.3892/mmr.2016.5327

Cited by 19 publications

(20 citation statements)

References 24 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…For instance, Jiang et al revealed that miR-495 overexpression suppresses osteosarcoma cell proliferation, colony formation, invasion and increased apoptosis in vitro (19). Studies showed that miR-495 upregulation inhibits cell proliferation and invasion and induces a metabolic shift in glioma (42)(43)(44). Formosa et al (36) and Li et al (45) indicated that the restored miR-495 expression attenuates prostate cancer cell growth and metastasis and promotes apoptosis in vitro.…”

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%

See 1 more Smart Citation

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

View full text Add to dashboard Cite

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.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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

View full text Add to dashboard Cite

show abstract

“…However, there are different views on the role of miR-495 in regulating tumor invasion and migration. 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.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-495 suppresses osteosarcoma invasion and migration by targeting HSP90AA1

Xiao¹,

Wang²,

Li³

et al. 2018

Oncotarget

View full text Add to dashboard Cite

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/

show abstract

“…Furthermore, we found that miR-495 could directly target Annexin A3 in CRC cells using the online database TargetScan 6.2. Currently, miR-495 has attracted much attention because several studies have reported that miR-495 is frequently decreased and functions as a tumor suppressor in gliomas as well as gastric and endometrial cancers [15-17], but it is increased and functions as an oncogene in breast and bladder cancers [18, 19]. However, until now, the level of miR-495 and its the precise mechanism in CRC have been unclear.…”

Section: Introductionmentioning

confidence: 99%

The MiR-495/Annexin A3/P53 Axis Inhibits the Invasion and EMT of Colorectal Cancer Cells

Bai¹,

Wang²,

Wang³

et al. 2017

Cell Physiol Biochem

View full text Add to dashboard Cite

Background/Aims: More and more reports have shown that the dysregulation of miRNAs can contribute to the progression and metastasis of human cancers. Many studies have shown that the down-regulation of the miR-495 level occurs in a variety of cancers, including colorectal cancer (CRC). However, the precise molecular mechanisms of miR-495 in CRC have not been well clarified. In the current study, we investigated the biological functions and molecular mechanisms of miR-495 in CRC cell lines. Methods: qRT-PCR was used to determine the level of miR-495 in CRC cell lines and tissues. A miR-495 mimic and inhibitor were transfected into CRC cells, and the effects of miR-495 on the invasion and EMT were explored by qRT-PCR as well as transwell and Western blot assays. Meanwhile, luciferase assays were performed to validate Annexin A3 as a miR-495 target in CRC cells. Results: In our study, we found that miR-495 is down-regulated in CRC tissues and cell lines. Moreover, the low level of miR-495 was associated with increased expression of Annexin A3 in CRC tissues and cell lines. The invasion and EMT of CRC cells were suppressed by the overexpression of miR-495. However, the down-regulation of miR-495 promoted the invasion and EMT of CRC cells. Bioinformatics analysis predicted that Annexin A3 was a potential target gene of miR-495. Next, the luciferase reporter assay confirmed that miR-495 could directly target Annexin A3. Consistent with the effect of miR-495, the down-regulation of Annexin A3 by siRNA inhibited the invasion and EMT of CRC cells through the up-regulation of p53. The introduction of Annexin A3 in CRC cells partially blocked the effects of the miR-495 mimic. Conclusion: The introduction of miR-495 directly targeted Annexin A3 to inhibit the invasion and EMT of CRC cells by up-regulating p53, and the down-regulation of Annexin A3 was essential for inhibiting the invasion and EMT of CRC cells by overexpressing miR-495. Overall, the re-activation of the miR-495/Annexin A3/ p53 axis may represent a new strategy for overcoming metastasis of CRC.

show abstract

Hsa-miR-495 acts as a tumor suppressor gene in glioma via the negative regulation of MYB

Cited by 19 publications

References 24 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

The MiR-495/Annexin A3/P53 Axis Inhibits the Invasion and EMT of Colorectal Cancer Cells

Contact Info

Product

Resources

About