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LINC02154 promotes cell cycle and mitochondrial function in oral squamous cell carcinoma
Takeshi Niinuma1, Hiroshi Kitajima1, Tatsuya Sato2,3
1Department of Molecular Biology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Cancer Science
|November 22, 2024
Summary
Long noncoding RNA LINC02154 promotes oral cancer by affecting cell cycle and mitochondrial function. Its upregulation correlates with poor prognosis, making it a potential therapeutic target for oral squamous cell carcinoma.
Area of Science:
- Oncology
- Molecular Biology
- Genomics
Background:
- Long noncoding RNAs (lncRNAs) are implicated in human cancers, but their role in oral squamous cell carcinoma (OSCC) is not fully understood.
- Investigating lncRNA expression in head and neck squamous cell carcinoma (HNSCC) can reveal novel oncogenic drivers.
Purpose of the Study:
- To investigate the role of lncRNAs in OSCC development and identify potential therapeutic targets.
- To elucidate the molecular mechanisms by which LINC02154 influences OSCC progression.
Main Methods:
- Analysis of The Cancer Genome Atlas (TCGA) dataset for lncRNA expression in HNSCC.
- In vitro and in vivo experiments involving LINC02154 knockdown in OSCC cell lines.
- RNA pulldown, mass spectrometry, and microRNA analysis to identify interacting proteins and regulatory pathways.
Main Results:
- Upregulation of LINC02154 in OSCC is associated with poorer prognosis.
- LINC02154 knockdown induces cell cycle arrest, apoptosis, and inhibits tumor growth.
- LINC02154 regulates FOXM1 expression via HNRNPK and affects mitochondrial function by interacting with LRPPRC.
Conclusions:
- LINC02154 acts as an oncogene in OSCC by modulating cell cycle progression and oxidative phosphorylation.
- LINC02154 is a promising therapeutic target for oral squamous cell carcinoma.
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