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MiR-150-3p targets SP1 and suppresses the growth of glioma cells
| Content Provider | Semantic Scholar |
|---|---|
| Author | Tan, Zhigang Jia, Jiaoying Jiang, Yugang |
| Copyright Year | 2018 |
| Abstract | Glioma has been considered as one of the most prevalent and common malignancy of the nervous system; however, the underlying mechanisms that are responsible for the occurrence and development of glioma still remain largely unknown. Amounting evidence highlights the critical regulatory function of miRNAs in carcinogenesis. Here, we showed that the expression of miR-150-3p was significantly decreased in glioma tissues and cell lines. Suppressed expression of miR-150-3p was associated with the lymph node metastasis of the glioma patients. Overexpression of miR-150-3p significantly inhibited the proliferation of glioma cells. Molecular study uncovered that the transcription factor specificity protein 1 (SP1) was identified as one of the targets of miR-150-3p Highly expressed miR-150-3p in glioma cells significantly decreased both the mRNA and protein levels of SP1. Consistently, the abundance of phosphatase and tension homolog deleted on chromosome ten (PTEN), a negative downstream target of SP1, was increased with the ectopic miR-150-3p Collectively, these results suggested that miR-150-3p suppressed the growth of glioma cells partially via regulating SP1 and possibly PTEN. |
| Starting Page | 93 |
| Ending Page | 108 |
| Page Count | 16 |
| File Format | PDF HTM / HTML |
| PubMed reference number | 29654167v1 |
| Alternate Webpage(s) | https://doi.org/10.1042/BSR20180019 |
| DOI | 10.1042/bsr20180019 |
| Journal | Bioscience reports |
| Volume Number | 38 |
| Language | English |
| Access Restriction | Open |
| Subject Keyword | Anatomic Node Body tissue CNS disorder Carcinogenesis Chromosome 3 Short Arm Cultured Cell Line Deletion (action) EBV-BART10-3p microRNA Ectopic Graft Glioma MIR150 wt Allele MicroRNAs Neoplasms Patients SP1 gene TRANSCRIPTION FACTOR Tension lymph node metastases lymph nodes |
| Content Type | Text |
| Resource Type | Article |
