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Updated: Dec 19, 2025

Induction of Mesenchymal-Epithelial Transitions in Sarcoma Cells
Published on: April 7, 2017
LncRNA MIR31HG functions as a ceRNA to regulate c-Met function by sponging miR-34a in esophageal squamous cell
Jie Chu1, Jinlin Jia1, Lijun Yang1
1Department of Medical Laboratory, The First Affiliated Hospital, Zhengzhou University, Zhengzhou, Henan Province, China.
Abstract:
Accumulating evidence has demonstrated that long non-coding RNAs (lncRNAs) function as essential regulators in the development and progression of multiple tumors. However, the molecular mechanisms of MIR31HG in regulating ESCC progression remain unknown. Here, we confirmed that MIR31HG facilitated ESCC cells proliferation in vivo. Besides, MIR31HG knockdown increases the percentage of cells at the G1 phase, along with reduced arrest in S phase and MIR31HG overexpression exhibits the opposite effects. Overexpressed MIR31HG decreases the percentage of apoptotic ESCC cells. Interestingly, MIR31HG can function as a competing endogenous RNA by sponging miR-34a. The rescue experiments demonstrated that MIR31HG function is partially reversed by inhibiting miR-34a. In addition, we found c-Met is a target gene of miR-34a and is indirectly regulated by MIR31HG. Taken together, our findings revealed that MIR31HG promotes ESCC progression by regulating miR-34a/ c-Met axis and may provide a new prospective for exploration and understanding of the biological effects of esophageal squamous cell carcinoma.
Insights
Long non-coding RNA MIR31HG promotes esophageal squamous cell carcinoma (ESCC) progression by regulating the miR-34a/c-Met axis. This study reveals MIR31HG
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Long non-coding RNAs (lncRNAs) are critical regulators in tumor development.
- The specific role of MIR31HG in esophageal squamous cell carcinoma (ESCC) progression is not well understood.
Purpose of the Study:
- To elucidate the molecular mechanisms by which MIR31HG influences ESCC progression.
- To investigate the regulatory relationship between MIR31HG, miR-34a, and c-Met in ESCC.
Main Methods:
- In vivo and in vitro experiments assessing cell proliferation and apoptosis.
- RNA interference (RNAi) techniques for gene knockdown and overexpression.
- Mechanism studies involving competing endogenous RNA (ceRNA) interactions and target gene validation.
Main Results:
- MIR31HG significantly promotes ESCC cell proliferation and inhibits apoptosis.
- MIR31HG acts as a competing endogenous RNA by sponging miR-34a.
- MIR31HG indirectly regulates c-Met expression through the miR-34a pathway, promoting ESCC progression.
Conclusions:
- MIR31HG promotes ESCC progression via the MIR31HG/miR-34a/c-Met axis.
- MIR31HG represents a potential therapeutic target for esophageal squamous cell carcinoma.
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