MicroRNA-646 inhibits proliferation and cell cycle progression of nasopharyngeal carcinoma cells by targeting mTOR
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Updated: Jan 4, 2026

Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis
Published on: March 30, 2019
1Department of Otolaryngology, The Seventh People's Hospital of Jinan, Jinan, China. 13953190521@163.com.
Objective:
To clarify whether microRNA-646 could regulate the proliferative potential and cell cycle progression of nasopharyngeal carcinoma cells through targeting mammalian target of rapamycin (mTOR). It, therefore, could influence the occurrence and progression of nasopharyngeal carcinoma.
Patients And Methods:
Quantitative Real-time polymerase chain reaction (qRT-PCR) was used to detect expression of the levels of microRNA-646 and mTOR in tumor tissues and paracancerous tissues of patients with nasopharyngeal carcinoma. Besides, their expressions in nasopharyngeal carcinoma cell lines were determined by qRT-PCR. Survival analysis was conducted to evaluate the sensitivity and specificity of microRNA-646 in diagnosing nasopharyngeal carcinoma. The overall survival of patients with nasopharyngeal carcinoma was calculated based on their expression levels of microRNA-646. The regulatory effects of microRNA-646 and mTOR on proliferative potential and cell cycle progression were explored by cell counting kit-8 (CCK-8) assay and flow cytometry, respectively. Dual-luciferase reporter gene assay was conducted to verify the relationship between microRNA-646 and mTOR, which was further confirmed by Pearson correlation analysis. Finally, gain-of-function experiments were carried out to determine whether microRNA-646 could regulate the proliferative potential and cell cycle progression of nasopharyngeal carcinoma cells by targeting mTOR.
Results:
MicroRNA-646 was lowly expressed in nasopharyngeal carcinoma tissues and cell lines. Survival analysis confirmed the diagnostic value of microRNA-646 in nasopharyngeal carcinoma. Besides, the nasopharyngeal carcinoma patients with high level of microRNA-646 were expected to have a longer 5-year survival time compared with those with low level. Overexpression of microRNA-646 inhibited the proliferative potential and cell cycle progression of HONE1 and SUNE1 nasopharyngeal carcinoma cells. Dual-luciferase reporter gene assay detected the binding of microRNA-646 to mTOR. Moreover, mTOR was highly expressed in nasopharyngeal carcinoma tissues and cell lines. A negative correlation was found between microRNA-646 and mTOR. That is, the overexpression of mTOR could reverse the inhibitory effects of microRNA-646 on the proliferative potential and cell cycle progression of HONE1 and SUNE1 cells.
Conclusions:
MicroRNA-646 remains a low level in nasopharyngeal carcinoma. It inhibits the proliferative potential and cell cycle progression of nasopharyngeal carcinoma cells by targeting mTOR. It can, therefore, inhibit the development of nasopharyngeal carcinoma.
Insights
MicroRNA-646 is downregulated in nasopharyngeal carcinoma and inhibits tumor growth by targeting mTOR. Upregulating microRNA-646 can suppress cancer cell proliferation and progression, offering a potential therapeutic strategy for nasopharyngeal carcinoma.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Nasopharyngeal carcinoma (NPC) is a prevalent cancer in certain regions.
- Understanding the molecular mechanisms regulating NPC progression is crucial for developing effective treatments.
Purpose of the Study:
- To investigate the role of microRNA-646 (miR-646) in regulating the proliferation and cell cycle of nasopharyngeal carcinoma cells.
- To determine if miR-646 targets the mammalian target of rapamycin (mTOR) pathway in NPC.
Main Methods:
- Quantitative Real-time polymerase chain reaction (qRT-PCR) to assess miR-646 and mTOR expression.
- Cell counting kit-8 (CCK-8) assay and flow cytometry to evaluate proliferation and cell cycle.
- Dual-luciferase reporter gene assay and Pearson correlation analysis to confirm the miR-646-mTOR interaction.
- Gain-of-function experiments to elucidate miR-646's regulatory role.
Main Results:
- MicroRNA-646 was significantly downregulated in NPC tissues and cell lines.
- Low miR-646 expression correlated with poorer survival in NPC patients.
- Overexpression of miR-646 inhibited NPC cell proliferation and induced cell cycle arrest.
- miR-646 directly targets mTOR, which was found to be upregulated in NPC.
- mTOR overexpression reversed the inhibitory effects of miR-646.
Conclusions:
- MicroRNA-646 acts as a tumor suppressor in nasopharyngeal carcinoma.
- miR-646 inhibits NPC cell proliferation and cell cycle progression by targeting mTOR.
- Restoring miR-646 levels may represent a therapeutic strategy for NPC.
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