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Updated: Dec 12, 2025

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
Published on: August 23, 2019
MiR-216a-5p inhibits tumorigenesis in Pancreatic Cancer by targeting TPT1/mTORC1 and is mediated by LINC01133
Jian Zhang1, Shuohui Gao2, Yandong Zhang1
1Department of Hepatobiliary and Pancreas Surgery, Jilin University First Hospital, Changchun, China.
Abstract:
MiR-216a-5p has opposite effects on tumorigenesis and progression in the context of different tumors, acting as either a tumor suppressor or an oncogene. However, the expression and function of miR-216a-5p in pancreatic cancer (PC) is not well characterized. In this study, we found miR-216a-5p was significantly downregulated in PC tissues and cell lines, which showed a negative correlation with peripancreatic lymph, perineural invasion and TNM stage of PCs patients. We made use of functional assays to reveal that miR-216a-5p inhibited growth and migration of PC cells in vitro and in vivo. Then, by employing the bioinformatics analysis and luciferase reporter assay, we demonstrated TPT1 was a potential target of miR-216a-5p, which contributes to tumor malignance by mediating mTORC1 pathway-associated autophagy. Furthermore, bioinformatics analysis and RNA pulldown confirmed that miR-216a-5p was mediated by LINC01133, which sponge miR-216a-5p, as a competing endogenous RNA (ceRNA). Collectively, our study revealed an important role of LINC01133/miR-216a-5p/TPT1 axis in the genesis and progression of PCs, which provides potential biomarkers for clinical diagnosis and therapy of PCs.
Insights
MicroRNA-216a-5p acts as a tumor suppressor in pancreatic cancer (PC), inhibiting growth and metastasis. Its downregulation is linked to advanced disease, suggesting potential diagnostic and therapeutic roles for the LINC01133/miR-216a-5p/TPT1 axis.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- MicroRNA-216a-5p exhibits context-dependent roles in tumorigenesis.
- Its specific function in pancreatic cancer (PC) remains largely uncharacterized.
Purpose of the Study:
- To investigate the expression and functional role of miR-216a-5p in pancreatic cancer.
- To elucidate the molecular mechanisms underlying miR-216a-5p's function in PC progression.
Main Methods:
- Analysis of miR-216a-5p expression in PC tissues and cell lines.
- In vitro and in vivo functional assays to assess cell growth and migration.
- Bioinformatics analysis, luciferase reporter assays, and RNA pulldown assays to identify targets and regulatory interactions.
Main Results:
- miR-216a-5p was significantly downregulated in PC tissues and correlated negatively with lymph node metastasis, perineural invasion, and TNM stage.
- miR-216a-5p suppressed PC cell growth and migration in vitro and in vivo.
- TPT1 was identified as a direct target of miR-216a-5p, mediating mTORC1 pathway-associated autophagy.
- LINC01133 was confirmed to act as a competing endogenous RNA (ceRNA) sponging miR-216a-5p.
Conclusions:
- The LINC01133/miR-216a-5p/TPT1 axis plays a critical role in the genesis and progression of pancreatic cancer.
- miR-216a-5p functions as a tumor suppressor in PC.
- This axis presents potential biomarkers for the clinical diagnosis and therapy of pancreatic cancer.
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