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Updated: Aug 15, 2026

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
Published on: August 23, 2019
CircRNA PVT1 promotes migration, invasion and glucose metabolism of thyroid cancer cells through modulating the
Huanli Hu1, Yanan Lu1, Yingchuan Sun2
1Medical College of Xuchang University, Xuchang City, 461000 Henan Province China.
Abstract:
This study aimed to investigate the biological functions and underlying molecular mechanisms of circular RNA plasmacytoma variant translocation 1 (circPVT1) in the progression of thyroid cancer.The expression levels of circPVT1 in thyroid tumor tissues and cell lines were compared to normal controls, and its association with clinicopathological features was analyzed. Functional assays were performed to assess the effects of circPVT1 silencing on thyroid cancer cell migration, invasion, and glucose metabolism. The interaction between circPVT1 and miR-195-5p was validated using bioinformatics prediction, RNA pull-down, dual-luciferase reporter assays, and RNA fluorescence in situ hybridization (FISH). The target relationship between miR-195-5p and pyruvate dehydrogenase kinase 4 (PDK4) was examined via luciferase reporter and Western blot assays. Rescue and epistasis experiments were conducted by restoring miR-195-5p expression or knocking down PDK4 in circPVT1-overexpressing cells. The role of the circPVT1/miR-195-5p/PDK4 axis was further validated in vivo using subcutaneous xenograft and experimental lung metastasis models.circPVT1 was significantly upregulated in thyroid tumors and cell lines, and its high expression correlated with advanced TNM stage and lymph node metastasis. Silencing circPVT1 suppressed migration, invasion, and glycolytic metabolism of thyroid cancer cells. Mechanistically, circPVT1 acted as a sponge for miR-195-5p, downregulating its expression, and miR-195-5p directly targeted and inhibited PDK4. Restoration of miR-195-5p or knockdown of PDK4 reversed the oncogenic phenotypes induced by circPVT1 overexpression. In vivo, circPVT1 promoted tumor growth and lung metastasis, which were attenuated by co-expression of miR-195-5p. Molecular analysis of lung metastases confirmed the dysregulation of the circPVT1/miR-195-5p/PDK4 axis within metastatic lesions.CircPVT1 promotes migration, invasion, glycolytic metabolism, and metastasis in thyroid cancer by sponging miR-195-5p and upregulating PDK4. These findings highlight the circPVT1/miR-195-5p/PDK4 axis as a potential therapeutic target for thyroid cancer intervention.
Supplementary Information:
The online version contains supplementary material available at 10.1007/s10616-026-00960-6.
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