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Updated: Oct 23, 2025
In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
Published on: August 23, 2019
Long Non-coding RNA RP11-395G23.3 Acts as a Competing Endogenous RNA of miR-124-3p to Regulate ROR1 in Anaplastic
An-Cheng Qin1,2, Yi Qian2, Yu-Yuan Ma2
1The Third Affiliated Hospital of Soochow University, Changzhou, China.
Abstract:
Anaplastic thyroid carcinoma (ATC) is one of the most aggressive human malignancies with poor prognosis. However, the underlying mechanisms of ATC remain to be elucidated. Recently, increasing studies have focused on competitive endogenous RNA (ceRNA) to discover valuable biomarkers for the diagnosis of ATC. The present study identified 705 differentially expressed mRNAs and 47 differentially expressed lncRNAs. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses were also conducted. Additionally, an lncRNA/miRNA/mRNA network was constructed which included 1103 regulatory relations. The upregulation of RP11-395G23.3 in ATC cells was confirmed by quantitative reverse transcription polymerase chain reaction (qRT-PCR). In the loss of function assays, results suggested silencing of RP11-395G23.3 inhibited cell proliferation and induced cell apoptosis. Mechanically, RP11-395G23.3 could increase ROR1 via sponging miR-124-3p as a ceRNA. Moreover, ROR1 expression was decreased with the downregulation of RP11-395G23.3, but was rescued by the co-transfection of the miR-124-3p inhibitor in ATC cells. Our research suggested that the RP11-395G23.3/miR-124-3p/ROR1 axis potentially acted as a potential target for the diagnosis of ATC.
Insights
Anaplastic thyroid carcinoma (ATC) research reveals RP11-395G23.3 promotes tumor growth by regulating miR-124-3p and ROR1. Silencing this long non-coding RNA inhibits ATC cell proliferation and induces apoptosis, suggesting a new diagnostic target.
Area of Science:
- Molecular Oncology
- Genomics
- Biomarker Discovery
Background:
- Anaplastic thyroid carcinoma (ATC) is an aggressive malignancy with poorly understood mechanisms.
- Competitive endogenous RNA (ceRNA) networks are emerging as crucial for identifying ATC biomarkers.
Purpose of the Study:
- To elucidate the molecular mechanisms of ATC and identify potential diagnostic biomarkers.
- To construct and analyze an lncRNA/miRNA/mRNA regulatory network in ATC.
Main Methods:
- Differential gene expression analysis (mRNAs and lncRNAs).
- Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses.
- Construction of an lncRNA/miRNA/mRNA network.
- Quantitative reverse transcription polymerase chain reaction (qRT-PCR) validation.
- Loss-of-function assays and mechanistic studies involving RP11-395G23.3, miR-124-3p, and ROR1.
Main Results:
- Identified 705 differentially expressed mRNAs and 47 differentially expressed lncRNAs.
- Constructed a network with 1103 regulatory relations.
- Confirmed RP11-395G23.3 upregulation in ATC; silencing inhibited proliferation and induced apoptosis.
- Established that RP11-395G23.3 acts as a ceRNA for miR-124-3p, upregulating ROR1.
Conclusions:
- The RP11-395G23.3/miR-124-3p/ROR1 axis is implicated in ATC pathogenesis.
- This axis represents a potential therapeutic target and diagnostic biomarker for anaplastic thyroid carcinoma.
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