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lncRNA KLF3-AS1 Suppresses Cell Migration and Invasion in ESCC by Impairing miR-185-5p-Targeted KLF3 Inhibition
Jun-Qi Liu1, Ming Deng2, Nan-Nan Xue1
1Department of Radiotherapy, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450000, P.R. China.
Molecular Therapy. Nucleic Acids
|March 21, 2020
Summary
Long non-coding RNA KLF3-AS1 inhibits esophageal squamous cell carcinoma (ESCC) progression by targeting miR-185-5p. Upregulating KLF3-AS1 reduces tumor growth and spread, offering a potential new treatment for ESCC.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Esophageal squamous cell carcinoma (ESCC) is a prevalent malignancy globally.
- Long non-coding RNAs (lncRNAs) play significant roles in cancer development, but their specific functions in ESCC are not fully understood.
Purpose of the Study:
- To investigate the role of lncRNA Krüppel-like factor 3 antisense RNA 1 (KLF3-AS1) in ESCC.
- To elucidate the regulatory mechanism of KLF3-AS1 involving miR-185-5p and KLF3 in ESCC.
Main Methods:
- Preparation and characterization of ESCC cell spheres with stem cell-like properties.
- Assessment of KLF3-AS1 expression in ESCC.
- Analysis of the interaction between KLF3-AS1, miR-185-5p, and KLF3.
- Evaluation of KLF3-AS1's effects on ESCC cell behaviors in vitro and tumor growth in vivo.
Main Results:
- KLF3-AS1 was found to be downregulated in ESCC.
- KLF3-AS1 upregulates KLF3 expression by binding to miR-185-5p, leading to decreased SOX2 and Oct4 expression.
- Upregulation of KLF3-AS1 inhibited ESCC cell colony formation, invasion, migration, and tumor volume, while promoting apoptosis.
Conclusions:
- lncRNA KLF3-AS1 acts as a tumor suppressor in ESCC.
- KLF3-AS1 inhibits ESCC progression by regulating the miR-185-5p/KLF3 axis.
- KLF3-AS1 represents a potential therapeutic target for ESCC treatment.
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