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MiR-130b can suppress proliferation of glioma cells through targeting PTEN to regulate AKT pathway.

AbstractPURPOSE:
To study the mechanism of action of micro ribonucleic acid (miR)-130b in the proliferation and apoptosis of glioma cells, and to determine whether it regulates the target gene phosphatase and tensin homolog deleted on chromosome ten (PTEN).
METHODS:
The endogenous expression of miR-130b was silenced via transfection with the miR-130b inhibitor. The effects of miR-130b silencing on the proliferation and apoptosis of LN229 cells were detected using cell counting kit-8 (CCK-8) assay, colony formation assay and flow cytometry. Whether miR-130b binds to the target gene PTEN was detected via luciferase reporter assay. The changes in the mRNA level of PTEN after miR-130b silencing were determined through quantitative reverse transcription-polymerase chain reaction (qRT-PCR). The effects of miR-130b on protein kinase B (AKT) signaling pathway-related proteins were determined through Western blotting, and the roles of miR-130b and PTEN in the proliferation of glioma cells were detected via CCK-8 assay.
RESULTS:
Compared with that in normal human astrocytes, the expression of miR-130b was significantly up-regulated in the three kinds of glioma cell lines (p<0.05). Silencing of miR-130b reduced the proliferation (p<0.05) and the colony formation of LN229 cells (p<0.05), and obviously increased their apoptosis (p<0.05), suggesting that silenced miR-130b is a growth inhibitor of glioma cells in vitro. The luciferase reporter assay confirmed that miR-130b directly bound to the 3'-untranslated region (3'UTR) of PTEN to suppress its expression. After transfection with the miR-130b inhibitor, both mRNA and protein expressions of PTEN were up-regulated (p<0.05). Moreover, after silencing of miR-130b, the phosphorylation of AKT was remarkably inhibited, while the cancer suppressor gene p27 was up-regulated.
CONCLUSIONS:
The carcinogenic effect of miR-130b in glioma was clarified in this study. Silencing of miR-130b may inhibit the AKT signaling pathway through up-regulating PTEN, thereby suppressing the proliferation of glioma cells.
AuthorsHaitao Niu, Yang Liu, Yanzhou Wang, Yong Tian, Hongsheng Jiang, Shuanzhu Cao, Ming Yang, Shaoquan Li
JournalJournal of B.U.ON. : official journal of the Balkan Union of Oncology (J BUON) 2020 Jul-Aug Vol. 25 Issue 4 Pg. 2059-2065 ISSN: 2241-6293 [Electronic] Cyprus
PMID33099953 (Publication Type: Journal Article)
Chemical References
  • MIRN130 microRNA, human
  • MicroRNAs
  • RNA, Messenger
  • Proto-Oncogene Proteins c-akt
  • PTEN Phosphohydrolase
  • PTEN protein, human
Topics
  • Apoptosis (physiology)
  • Astrocytes (metabolism)
  • Brain Neoplasms (genetics, metabolism, pathology)
  • Cell Line, Tumor
  • Cell Proliferation (physiology)
  • Glioma (genetics, metabolism, pathology)
  • Humans
  • MicroRNAs (biosynthesis, genetics, metabolism)
  • PTEN Phosphohydrolase (genetics, metabolism)
  • Proto-Oncogene Proteins c-akt (metabolism)
  • RNA, Messenger (genetics, metabolism)
  • Signal Transduction
  • Up-Regulation

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