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Updated: Aug 5, 2025

Modeling Oral-Esophageal Squamous Cell Carcinoma in 3D Organoids
Published on: December 23, 2022
LINC01116 modulates EMT process via binding with AGO1 mRNA in oesophageal squamous cell carcinoma
Xin Fang1, Li-Hua Ren2, Sachin Mulmi Shrestha1
1Medical College, Southeast University, Nanjing 210009, Jiangsu Province, China.
Abstract:
Recent researches have uncovered that long non-coding RNAs (lncRNAs) are closely correlated with the development of different diseases, while biological functions and hidden molecular mechanisms of antisense lncRNAs in oesophageal squamous cell carcinoma (OSCC) remain unclear. Here, we identified upregulation of LINC01116 in RNA sequencing data, online database, and in OSCC and intraepithelial neoplasia (IEN) specimens. Functionally, LINC01116 facilitates OSCC advancement and metastasis in vitro and vivo. Mechanistically, elevated expression of LINC01116 in OSCC cells other than tumor stroma and cytoplasmic enables it to activate AGO1 expression via complementary binding with AGO1 mRNA to facilitate EMT process of OSCC.
Insights
Long non-coding RNA LINC01116 promotes esophageal squamous cell carcinoma (OSCC) progression and metastasis. It activates AGO1 expression, driving the epithelial-mesenchymal transition (EMT) process in OSCC cells.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Long non-coding RNAs (lncRNAs) are implicated in various diseases.
- The specific roles and mechanisms of antisense lncRNAs in esophageal squamous cell carcinoma (OSCC) are not fully understood.
Purpose of the Study:
- To investigate the role and molecular mechanism of LINC01116 in the development and progression of OSCC.
Main Methods:
- Analysis of RNA sequencing data and online databases.
- Validation of LINC01116 expression in OSCC and intraepithelial neoplasia (IEN) specimens.
- In vitro and in vivo functional assays to assess LINC01116's impact on OSCC progression and metastasis.
- Investigation of the molecular mechanism involving AGO1 activation and epithelial-mesenchymal transition (EMT).
Main Results:
- LINC01116 was found to be upregulated in OSCC and IEN tissues.
- Overexpression of LINC01116 promoted OSCC cell proliferation, migration, and invasion in vitro and tumor growth and metastasis in vivo.
- LINC01116, predominantly expressed in OSCC cells (cytoplasmic), activates AGO1 expression by binding to AGO1 mRNA.
- This activation facilitates the EMT process, contributing to OSCC progression.
Conclusions:
- LINC01116 is an oncogenic lncRNA that promotes OSCC progression and metastasis.
- The mechanism involves LINC01116-induced AGO1 activation and subsequent EMT.
- LINC01116 may serve as a potential diagnostic biomarker and therapeutic target for OSCC.
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