Cited by 191MicroRNA in disease regulationCancer-related molecular mechanisms researchHead and Neck Cancer Studies

Regulation of the cell cycle gene, BTG2, by miR-21 in human laryngeal carcinoma

Liu, Min, Wu, Haidong, Liu, Tao, Li, Yixuan, Wang, Fang, Wan, Haiying, Li, Xin, Tang, Hua·2009·Cell Research

Abstract

MicroRNAs are short regulatory RNAs that negatively modulate gene expression at the post-transcriptional level, and are deeply involved in the pathogenesis of several types of cancers. To investigate whether specific miRNAs and their target genes participate in the molecular pathogenesis of laryngeal carcinoma, oligonucleotide microarrays were used to assess the differential expression profiles of microRNAs and mRNAs in laryngeal carcinoma tissues compared with normal tissues. The oncogenic miRNA, microRNA-21 (miR-21), was found to be upregulated in laryngeal carcinoma tissues. Knockdown of miR-21 by specific antisense oligonucleotides inhibited the proliferation potential of HEp-2 cells, whereas overexpression of miR-21 elevated growth activity of the cells, as detected by the colony formation assay. The cell number reduction caused by miR-21 inhibition was due to the loss of control of the G1-S phase transition, instead of a noticeable increase in apoptosis. Subsequently, a new target gene of miR-21, BTG2, was found to be downregulated in laryngeal carcinoma tissues. BTG2 is known to act as a pan-cell cycle regulator and tumor suppressor. These findings indicate that aberrant expression of miR-21 may contribute to the malignant phenotype of laryngeal carcinoma by maintaining a low level of BTG2. The identification of the oncogenic miR-21 and its target gene, BTG2, in laryngeal carcinoma is potentially valuable for cancer diagnosis and therapy.

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Crossref · 10.1038/cr.2009.72

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  • In laryngeal carcinoma, miR-21 targets BTG2, a p53 target gene, recently shown to suppress oncogenic Ras activity by reducing the GTP bound, active state.

    “In laryngeal carcinoma, miR-21 targets BTG2 (Liu et al., 2009), a p53 target gene, recently shown to suppress oncogenic Ras activity by reducing the GTP bound, active state (Buganim et al., 2010).”

    From Modulation of K-Ras-Dependent Lung Tumorigenesis by MicroRNA-21 (2010) · cites this paper as Liu et al., 2009

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Authors
Liu, M., Wu, H., Liu, T., Li, Y., Wang, F., Wan, H., Li, X., & Tang, H.
Affiliations
Tianjin Medical University (CN)
Corresponding author
Tang, Hua
Venue
Cell Research
Published
2009-06-23
Volume
19
Issue
7
Pages
828-837
ISSN
  • 1001-0602 (ISSN-L)
  • 1748-7838
OpenAlex
W2083966895
Cited by
189
References
33
Citations by year
2026: 6 · 2025: 4 · 2024: 7 · 2023: 6 · 2022: 6 · 2021: 18 · 2020: 11 · 2019: 4 · 2018: 11 · 2017: 10 · 2016: 14 · 2015: 20 · 2014: 20 · 2013: 8 · 2012: 14
FWCI
4.92
Type
journal article
Language
en
Open access
closed
Locations
  • Cell Research (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Natural Science Foundation of China (30873017)
  • Tianjin Medical University
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 › Otorhinolaryngology › Head and Neck Cancer Studies
Keywords
miR-21, BTG2, laryngeal cancer, miRNA target genes, cell cycle regulation, G1/S transition, tumor suppressor, cell proliferation, HEp-2 cells, post-transcriptional regulation, oncogenic microRNA
MeSH terms
Carcinoma, Humans, Laryngeal Neoplasms, Down-Regulation, Gene Expression Regulation, Neoplastic, G1 Phase, S Phase, Oligonucleotides, Antisense, Immediate-Early Proteins, Tumor Suppressor Proteins, MicroRNAs, Cell Line, Tumor, Gene Knockdown Techniques

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