Cited by 109MicroRNA in disease regulationGlioma Diagnosis and TreatmentCancer-related molecular mechanisms research

MiR-125b acts as an oncogene in glioblastoma cells and inhibits cell apoptosis through p53 and p38MAPK-independent pathways

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Wu, N, Lin, X, Zhao, X, Zheng, L, Xiao, L, Liu, J, Ge, L, Cao, S·2013·British Journal of Cancer

Abstract

BACKGROUND: We have recently identified miR-125b upregulation in glioblastoma (GMB). The aim of this study is to determine the correlation between miR-125b expression and malignant grades of glioma and the genes targeted by miR-125b. METHODS: Real-time PCR was employed to measure the expression level of miR-125b. Cell viability was evaluated by cell growth and colony formation in soft-agar assays. Cell apoptosis was determined by Hoechst 33342 staining and AnnexinV-FITC assay. The Luciferase assay was used to confirm the actual binding sites of p38MAPK mRNA. Western blot was used to detect the gene expression level. RESULTS: The expression level of miR-125b is positively correlated with the malignant grade of glioma. Ectopic expression of miR-125b promotes the proliferation of GMB cells. Knockdown of endogenous miR-125b inhibits cell proliferation and promotes cell apoptosis. Further studies reveal that p53 is regulated by miR-125b. However, downregulation of the endogenous miR-125b also results in p53-independent apoptotic pathway leading to apoptosis in p53 mutated U251 cells and p53 knockdown U87 cells. Moreover, p38MAPK is also regulated by miR-125b and downregulation of miR-125b activates the p38MAPK-induced mitochondria apoptotic pathway. CONCLUSION: High-level expression of miR-125b is associated with poor outcomes of GMB. MiR-125b may have an oncogenic role in GMB cells by promoting cell proliferation and inhibiting apoptosis.

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  • P53 is regulated by miR-125b, an oncogenic miRNA that is upregulated in glioblastoma and that inhibits cell proliferation and promotes evasion of apoptosis.

    “P53 is in turn regulated by miR-125b, an oncogenic miRNA that is upregulated in GBM and that inhibits cell proliferation and promotes evasion of apoptosis [52].”

    From The p53 Pathway in Glioblastoma (2018) · cites this paper as [52]

    The Results report that miR-125b regulates p53, and the Discussion describes its upregulation in glioblastoma tissue. But the claim reverses the proliferation finding: the Results say miR-125b promotes cell proliferation, while its knockdown inhibits proliferation and promotes apoptosis. Page numbers are unavailable in our copy. (LLM, conf=0.90)

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Authors
Wu, N., Lin, X., Zhao, X., Zheng, L., Xiao, L., Liu, J., Ge, L., & Cao, S.
Affiliations
  • Chinese Academy of Sciences (CN)
  • Capital Medical University (CN)
  • Qingdao University (CN)
  • Yellow Sea Fisheries Research Institute (CN)
  • Qingdao Agricultural University (CN)
  • Roswell Park Comprehensive Cancer Center (US)
Corresponding author
  • Lin, X
  • Cao, S
Venue
British Journal of Cancer
Published
2013-10-29
Volume
109
Issue
11
Pages
2853-2863
ISSN
  • 0007-0920 (ISSN-L)
  • 1532-1827
OpenAlex
W2008006957
Cited by
109
References
39
Citations by year
2025: 8 · 2024: 2 · 2023: 9 · 2022: 6 · 2021: 7 · 2020: 30 · 2019: 5 · 2018: 8 · 2017: 4 · 2016: 12 · 2015: 13 · 2014: 5
FWCI
3.52
Type
journal article
Language
en
Open access
Locations
  • British Journal of Cancer (publishedVersion, cc-by-nc-sa)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-sa)
  • PubMed Central (publishedVersion, cc-by-nc-sa)
  • PubMed (publishedVersion)
Funders
National Natural Science Foundation of China (81273550, 81072065, 41306157)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
  • Health Sciences › Medicine › Genetics › Glioma Diagnosis and Treatment
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer-related molecular mechanisms research
Keywords
miR-125b, glioblastoma, oncogenic microRNA, apoptosis, p53, p38 MAPK, mitochondrial apoptosis, cell proliferation, tumor grade, TP53 mutation, microRNA target regulation
MeSH terms
Adolescent, Adult, Aged, Animals, Brain Neoplasms, Cells, Cultured, Child, Female, Glioblastoma, Humans, Male, Middle Aged, Oncogenes, Signal Transduction, Tumor Suppressor Protein p53, Apoptosis, MicroRNAs, p38 Mitogen-Activated Protein Kinases, Rats, Young Adult, HEK293 Cells

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