Cited by 86MicroRNA in disease regulationCancer-related molecular mechanisms researchGlioma Diagnosis and Treatment

MicroRNA-106b-5p boosts glioma tumorigensis by targeting multiple tumor suppressor genes

Liu, F, Gong, J, Huang, W, Wang, Z, Wang, M, Yang, J, Wu, C, Wu, Z +1 more·2014·Oncogene

Abstract

Aberrant expression of microRNAs (miRNAs) has been implicated in cancer initiation and progression. However, little is known about the potential role of miRNAs in glioma tumorigenesis. In this study, we found that miRNA-106b-5p was significantly upregulated in glioma tumor samples and cell lines compared with normal brain tissues, and its expression level correlated with the pathological grading. Overexpression of miR-106b-5p in glioma tumor cells significantly promoted cell proliferation, although inhibited cell apoptosis in vitro and in vivo. In contrast, knockdown of miR-106b-5p significantly inhibited cell proliferation, although enhanced cell apoptosis. Mechanistic study revealed that two target genes, retinoblastoma-like 1 (RBL1) and RBL2, were involved in miR-106b-5p's regulation of cell proliferation and one target gene, caspase-8 (CASP8), mediated miR-106b-5p's regulation of apoptosis. We also investigated the function of the three targets in glioma tumorigenesis by RNA interference manipulation and demonstrated that knockdown of these target genes led to cell proliferation enhancement or cell apoptosis inhibition in vitro. More interestingly, the expression levels of these targets were significantly downregulated in glioma samples and knockdown of these targets in glioma cells inhibited the xenograft tumor formation in vivo. Moreover, we verified the regulation function of miR-106b-5p and its targets on cell proliferation and apoptosis of the primary cultured astrocytes isolated from glioma tumor samples and healthy controls. Collectively, our findings show the critical roles of miR-106b-5p and its targets, RBL1, RBL2 and CASP8, in glioma tumorigenesis and provide potential candidates for malignant glioma therapy.

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Crossref · 10.1038/onc.2013.428

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Authors
Liu, F., Gong, J., Huang, W., Wang, Z., Wang, M., Yang, J., Wu, C., Wu, Z., & Han, B.
Affiliations
  • Changzhou No.2 People's Hospital (CN)
  • First Affiliated Hospital of Soochow University (CN)
Corresponding author
  • Huang, W
  • Wang, Z
Venue
Oncogene
Published
2013-10-28
Volume
33
Issue
40
Pages
4813-4822
ISSN
  • 0950-9232 (ISSN-L)
  • 1476-5594
OpenAlex
W2030857870
Cited by
86
References
31
Citations by year
2026: 1 · 2025: 2 · 2024: 4 · 2023: 6 · 2022: 7 · 2021: 8 · 2020: 14 · 2019: 6 · 2018: 7 · 2017: 7 · 2016: 13 · 2015: 8 · 2014: 3
FWCI
2.81
Type
journal article
Language
en
Open access
closed
Locations
  • Oncogene (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • World Health Organization
  • Chinese Academy of Sciences
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer-related molecular mechanisms research
  • Health Sciences › Medicine › Genetics › Glioma Diagnosis and Treatment
Keywords
miR-106b-5p, glioma, carcinogenesis, RBL1, RBL2, caspase-8, tumor suppressor, cell proliferation, apoptosis, astrocytes, tumor grade, xenograft tumor formation, microRNA therapeutic target
MeSH terms
Animals, Brain Neoplasms, Female, Glioblastoma, Humans, Mice, Inbred BALB C, Mice, Nude, Neoplasm Transplantation, Gene Expression, Gene Expression Regulation, Neoplastic, Genes, Tumor Suppressor, Apoptosis, RNA Interference, MicroRNAs, Cell Line, Tumor, Tumor Burden, Cell Proliferation, Retinoblastoma-Like Protein p130, Retinoblastoma-Like Protein p107, Mice, Caspase 8, HEK293 Cells, Carcinogenesis

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