Related Experiment Video
Updated: Feb 21, 2026

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
Published on: August 23, 2019
MiR-206 inhibits Head and neck squamous cell carcinoma cell progression by targeting HDAC6 via PTEN/AKT/mTOR pathway
Fangzhou Liu1, Xiaotong Zhao2, Yichun Qian1
1Department of Head and Neck Surgery, Jiangsu Cancer Hospital, Jiangsu Institute of Cancer Research, Nanjing Medical University Affiliated Cancer Hospital, Nangjing 210000, China.
Abstract:
As a kind of endogenous noncoding small RNA, microRNA (miRNA) plays important roles of regulation to various physiological functions, while its affections on senescence of human Head and neck squamous cell carcinoma (HNSCC) are still unknown. The objective of this study was to investigate the effect of miR-206 in HNSCC tissues, adjacent normal tissues and cell lines, and explore its biological functions in HNSCC. In our study, the level of miR-206 in HNSCC tissues and adjacent normal tissues was detected via real-time qPCR. The effect of miR-206 on cell proliferation was tested by MTT assay, colony formation and cell cycle assays. In order to explore the effect of miR-206 on HNSCC cell migration and invasion, we performed wound healing assays and transwell assays. Luciferase reporter assays were designed to identify the interaction between 3'UTR of HDAC6 and miR-206. The level of signaling pathway-related proteins was determined by western blot. The expression of miR-206 was found to be observably decreased in HNSCC tissues and cell lines through real time-PCR. Restoration of miR-206 weaked cell proliferation, invasion and migration in HNSCC cells and the cell cycle was arrest in S phase. Further explores have shown that miR-206 could inhibit HNSCC cells proliferation by targeting the HDAC6 via PTEN/AKT/mTOR pathway. Taken together, our results demonstrated that miR-206 plays a critical role in HNSCC progression by targeting HDAC6 via PTEN/AKT/mTOR pathway, which might be a potential target for diagnostic and therapeutic in HNSCC.
Insights
MicroRNA-206 (miR-206) is decreased in Head and Neck Squamous Cell Carcinoma (HNSCC). Restoring miR-206 inhibits HNSCC cell proliferation, migration, and invasion by targeting HDAC6, offering a potential therapeutic target.
Area of Science:
- Oncology
- Molecular Biology
- Gene Regulation
Background:
- MicroRNAs (miRNAs) are endogenous noncoding small RNAs regulating physiological functions.
- The role of miRNAs in Head and Neck Squamous Cell Carcinoma (HNSCC) senescence remains largely unknown.
- This study investigates the function of miR-206 in HNSCC.
Purpose of the Study:
- To determine the expression level of miR-206 in HNSCC tissues and cell lines.
- To explore the biological functions of miR-206 in HNSCC progression, including proliferation, migration, and invasion.
- To elucidate the molecular mechanism by which miR-206 exerts its effects in HNSCC.
Main Methods:
- Real-time quantitative PCR (qPCR) to measure miR-206 expression.
- MTT assay, colony formation, and cell cycle analysis to assess proliferation.
- Wound healing and Transwell assays to evaluate migration and invasion.
- Luciferase reporter assays to confirm targeting of HDAC6.
- Western blot to analyze signaling pathway proteins (PTEN/AKT/mTOR).
Main Results:
- miR-206 expression was significantly decreased in HNSCC tissues and cell lines compared to normal controls.
- Restoration of miR-206 inhibited HNSCC cell proliferation, migration, and invasion.
- miR-206 induced S-phase cell cycle arrest in HNSCC cells.
- miR-206 directly targets the 3'UTR of HDAC6.
- miR-206 inhibits HNSCC progression by targeting HDAC6 through the PTEN/AKT/mTOR pathway.
Conclusions:
- miR-206 plays a crucial role in HNSCC progression.
- miR-206 acts as a tumor suppressor in HNSCC by targeting HDAC6 via the PTEN/AKT/mTOR pathway.
- miR-206 represents a potential diagnostic and therapeutic target for HNSCC.
Related Concept Videos
mTOR Signaling and Cancer Progression
The mTOR pathway or the...
PI3K/mTOR/AKT Signaling Pathway
Inhibition of Cdk Activity
MicroRNAs
MicroRNAs
Abnormal Proliferation

