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Updated: Jun 3, 2026

Genome-wide Screen for miRNA Targets Using the MISSION Target ID Library
Published on: April 6, 2012
miR-1 as a tumor suppressive microRNA targeting TAGLN2 in head and neck squamous cell carcinoma
Nijiro Nohata1, Yaeko Sone, Toyoyuki Hanazawa
1Department of Functional Genomics, Chiba University Graduate School of Medicine, Chiba, Japan.
Abstract:
Based on the microRNA (miRNA) expression signatures of hypopharyngeal and esophageal squamous cell carcinoma, we found that miR-1 was significantly down-regulated in cancer cells. In this study, we investigated the functional significance of miR-1 in head and neck squamous cell carcinoma (HNSCC) cells and identified miR-1-regulated novel cancer pathways. Gain-of-function studies using miR-1 revealed significant decreases in HNSCC cell proliferation, invasion, and migration. In addition, the promotion of cell apoptosis and cell cycle arrest was demonstrated following miR-1e transfection of cancer cells. A search for the targets of miR-1 revealed that transgelin 2 (TAGLN2) was directly regulated by miR-1. Silencing of TAGLN2 significantly inhibited cell proliferation and invasion in HNSCC cells. Down-regulation of miR-1 and up-regulation of TAGLN2 were confirmed in HNSCC clinical specimens. Our data indicate that TAGLN2 may have an oncogenic function and may be regulated by miR-1, a tumor suppressive miRNA in HNSCC. The identification of novel miR-1-regulated cancer pathways could provide new insights into potential molecular mechanisms of HNSCC carcinogenesis.
Insights
MicroRNA-1 (miR-1) acts as a tumor suppressor in head and neck squamous cell carcinoma (HNSCC). It inhibits cancer cell proliferation and invasion by targeting transgelin 2 (TAGLN2), a potential oncogene.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- MicroRNA (miRNA) expression profiling identified miR-1 as significantly downregulated in hypopharyngeal and esophageal squamous cell carcinoma.
- Head and neck squamous cell carcinoma (HNSCC) is a complex malignancy with poorly understood molecular drivers.
Purpose of the Study:
- To investigate the functional role of miR-1 in HNSCC.
- To identify novel cancer-related pathways regulated by miR-1.
- To elucidate the relationship between miR-1 and its potential targets in HNSCC.
Main Methods:
- Gain-of-function studies involving miR-1 transfection in HNSCC cells.
- Analysis of cell proliferation, invasion, migration, apoptosis, and cell cycle.
- Identification and validation of miR-1 targets using molecular assays.
- Analysis of miR-1 and TAGLN2 expression in HNSCC clinical specimens.
Main Results:
- miR-1 transfection significantly reduced HNSCC cell proliferation, invasion, and migration.
- miR-1 promoted apoptosis and induced cell cycle arrest in HNSCC cells.
- Transgelin 2 (TAGLN2) was identified as a direct target of miR-1; TAGLN2 silencing inhibited HNSCC cell proliferation and invasion.
- Downregulation of miR-1 and upregulation of TAGLN2 were observed in HNSCC clinical samples.
Conclusions:
- miR-1 functions as a tumor suppressor miRNA in HNSCC.
- TAGLN2 exhibits oncogenic properties in HNSCC and is negatively regulated by miR-1.
- The miR-1/TAGLN2 axis represents a novel pathway implicated in HNSCC development and progression, offering potential therapeutic targets.
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