Suppression of MIR31HG affects the functional properties of thyroid cancer cells depending on the miR-761/MAPK1 axis
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Updated: Sep 26, 2025

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
Published on: August 23, 2019
Shuwang Peng1, Luyang Chen2, Zhengtai Yuan3
1Department of Gastrointestinal and Thyroid and Vascular Surgery, The First Hospital of Hunan University of Chinese Medicine, Ward 22, 13th floor, Zhihe Building, No.95 Shaoshan Middle Road, Yuhua District, Changsha, 410000, Hunan, Province, China. pengshuwang@126.com.
Background:
Thyroid cancer is the most prevalent endocrine malignancy. Long non-coding RNA (lncRNA) MIR31HG is abnormally expressed in thyroid cancer tissues. However, the precise, critical role of MIR31HG in thyroid cancer development remains unclear.
Methods:
MIR31HG, microRNA (miR)-761 and mitogen-activated protein kinase 1 (MAPK1) were quantified by quantitative real-time PCR (qRT-PCR) and immunoblotting. Cell viability, proliferation, apoptosis, invasion and migration abilities were evaluated by MTS, 5-Ethynyl-2'-Deoxyuridine (EdU), flow cytometry, transwell and wound-healing assays, respectively. Dual-luciferase reporter assays were used to validate the direct relationship between miR-761 and MIR31HG or MAPK1.
Results:
MIR31HG was overexpressed in human thyroid cancer, and its overexpression predicted poor prognosis. Suppression of MIR31HG impeded cell proliferation, invasion and migration, as well as promoted cell apoptosis in vitro, and diminished the growth of xenograft tumors in vivo. Mechanistically, MIR31HG targeted and regulated miR-761. Moreover, miR-761 was identified as a molecular mediator of MIR30HG function in regulating thyroid cancer cell behaviors. MAPK1 was established as a direct and functional target of miR-761 and MAPK1 knockdown phenocopied miR-761 overexpression in impacting thyroid cancer cell behaviors. Furthermore, MIR31HG modulated MAPK1 expression by competitively binding to miR-761 via the shared binding sequence.
Conclusion:
Our findings demonstrate that MIR31HG targets miR-761 to regulate the functional behaviors of thyroid cancer cells by upregulating MAPK1, highlighting a strong rationale for developing MIR31HG as a novel therapeutic target against thyroid cancer.
Insights
Long non-coding RNA MIR31HG promotes thyroid cancer by targeting miR-761 and upregulating MAPK1. Inhibiting MIR31HG offers a potential therapeutic strategy for thyroid cancer treatment.
Area of Science:
- Molecular Biology
- Oncology
- Genetics
Background:
- Thyroid cancer is a common endocrine malignancy.
- Long non-coding RNA (lncRNA) MIR31HG is dysregulated in thyroid cancer.
- The exact role of MIR31HG in thyroid cancer pathogenesis is not fully understood.
Purpose of the Study:
- To elucidate the functional role of MIR31HG in thyroid cancer.
- To investigate the molecular mechanisms underlying MIR31HG's action.
- To assess MIR31HG as a potential therapeutic target for thyroid cancer.
Main Methods:
- Quantitative real-time PCR and immunoblotting to measure MIR31HG, miR-761, and MAPK1 levels.
- In vitro assays (MTS, EdU, flow cytometry, transwell, wound-healing) to assess cell behavior.
- Dual-luciferase reporter assays to confirm direct interactions.
Main Results:
- MIR31HG overexpression in thyroid cancer correlates with poor prognosis.
- MIR31HG suppression inhibits proliferation, invasion, migration, and promotes apoptosis.
- MIR31HG targets miR-761, which in turn targets MAPK1, creating a regulatory axis.
Conclusions:
- MIR31HG promotes thyroid cancer progression by upregulating MAPK1 via sponging miR-761.
- MIR31HG represents a promising novel therapeutic target for thyroid cancer.
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