Aberrant DNA hypermethylation-silenced LINC00886 gene accelerates malignant progression of laryngeal carcinoma
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Updated: Dec 27, 2025
Comprehensive DNA Methylation Analysis Using a Methyl-CpG-binding Domain Capture-based Method in Chronic Lymphocytic Leukemia Patients
Published on: June 16, 2017
Lili Lan1, Huan Cao2, Weiwei Chi3
1Otolaryngology Head and Neck Surgery Department, The Second Hospital of Hebei Medical University, Shijiazhuang 050005, Hebei, China; Otolaryngology Head and Neck Surgery Department, The Fourth Hospital of Hebei Medical University, Shijiazhuang 050011, Hebei, China.
Background:
Long noncoding RNAs (lncRNAs) play crucial role in formation and progression of tumors. DNA methylation has become increasingly recognized as a frequent event of epigenetic alterations and one of the primary mechanisms of gene inactivation. The research aims to investigate the biofunction of a novel lncRNA in LSCC.
Methods:
qRT-PCR, BGS, and MSP methods were employed to measure the relative expression level and methylation status of LINC00886. Additionally, we examined the effects of LINC00886 on cells proliferation and invasion using LINC00886 over-expression. Nude mouse xenograft models were conducted to assess LINC00886 effects on LSCC growth in vivo. High-throughput sequencing technology and Western blot assay were carried out to have an in-depth study of the downstream target genes and signaling pathways in which LINC00886 may participate.
Results:
The remarkable downregulation of LINC00886 was observed in tumor tissues and laryngeal cancer cell lines. The significant decrease of LINC00886 was correlated with pathological grade in LSCC tissues. The expression level of LINC00886 in laryngeal cancer cell lines was significantly reversed by 5-Aza-dC. The occurrence of aberrant methylation events in the LINC00886 TSS was more responsible for the down-expression of LINC00886. Over-expression of LINC00886 dramatically mitigated cell proliferation, migration, and invasion in vitro as well as suppressed tumor growth in vivo. LINC00886 may be associated with VEGFA/PI3K/AKT signaling pathways and epithelial-mesenchymal transition (EMT) process.
Conclusions:
We provide the first evidence of the involvement of LINC00886 in laryngeal carcinoma, which was downregulated due to methylation of the promoter region and served as tumor suppressor genes. LINC00886 is expected to become a novel biomarker in laryngeal carcinoma.
Insights
Long noncoding RNA LINC00886 acts as a tumor suppressor in laryngeal squamous cell carcinoma (LSCC). Its downregulation, caused by promoter methylation, inhibits LSCC progression and may serve as a novel diagnostic biomarker.
Area of Science:
- Oncology
- Epigenetics
- Molecular Biology
Background:
- Long noncoding RNAs (lncRNAs) are implicated in tumor development.
- DNA methylation is a key epigenetic mechanism for gene silencing in cancer.
- Laryngeal squamous cell carcinoma (LSCC) progression involves complex molecular alterations.
Purpose of the Study:
- To investigate the functional role of the novel lncRNA LINC00886 in LSCC.
- To determine the regulatory mechanisms, including DNA methylation, affecting LINC00886 expression.
- To assess the therapeutic potential of LINC00886 in LSCC.
Main Methods:
- Quantitative reverse transcription-PCR (qRT-PCR) and methylation-specific techniques (BGS, MSP) were used to analyze LINC00886 expression and methylation.
- In vitro cell proliferation and invasion assays were performed following LINC00886 overexpression.
- Nude mouse xenograft models evaluated LINC00886's in vivo effects on tumor growth.
- High-throughput sequencing and Western blot identified downstream targets and pathways.
Main Results:
- LINC00886 was significantly downregulated in LSCC tissues and cell lines, correlating with pathological grade.
- Aberrant promoter methylation was identified as the primary cause of LINC00886 downregulation, reversible with 5-Aza-dC treatment.
- Overexpression of LINC00886 suppressed LSCC cell proliferation, migration, and invasion in vitro and inhibited tumor growth in vivo.
- LINC00886 may influence the VEGFA/PI3K/AKT signaling pathway and epithelial-mesenchymal transition (EMT).
Conclusions:
- LINC00886 functions as a tumor suppressor in laryngeal carcinoma.
- Promoter methylation-induced downregulation of LINC00886 contributes to LSCC progression.
- LINC00886 represents a potential novel biomarker for laryngeal carcinoma diagnosis and prognosis.
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