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Updated: Dec 20, 2025

Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis
Published on: March 30, 2019
Long non-coding RNA DNM3OS/miR-204-5p/HIP1 axis modulates oral cancer cell viability and migration
Xiaodan Fang1, Zhangui Tang1, Haixia Zhang2
1Department of Oral and Maxillofacial Surgery, Xiangya Stomatological Hospital, Central South University, Changsha, Hunan, China.
Background:
Non-coding RNAs play a critical role in the occurrence and development of oral cancer. The present study is aimed to identify long non-coding RNA (lncRNA) that might be novel effective targets for the treatments of oral cancer and the underlying mechanism.
Methods:
The microarray profiling and RNA-sequencing analysis were performed to identify lncRNAs related to oral cancer development, and lncRNA DNM3OS was selected. DNM3OS knockdown was generated in cancer cell lines, and the specific effects of DNM3OS knockdown on cell phenotype were examined. DNM3OS targeted miRNA and miRNA targeted downstream mRNA were selected, the predicted bindings were verified, and the specific effects of miRNA on oral cancer cells were examined. Finally, the dynamic effects of DNM3OS and miRNA on target mRNA expression and oral cancer cell phenotype were examined.
Results:
DNM3OS was upregulated in oral cancer tissues and cells. DNM3OS knockdown in CAL27 and SCC-9 cells inhibited cell viability and migration. DNM3OS targeted miR-204-5p to inhibit miR-204-5p expression. miR-204-5p overexpression suppressed oral cancer cell aggressiveness. miR-204-5p targeted HIP1 to inhibit HIP1 expression. HIP1 knockdown inhibited oral cancer cell viability and migration. The effects of DNM3OS knockdown were significantly reversed by miR-204-5p inhibition. Within oral carcinoma tissue samples, expression of DNM3OS and HIP1 was increased whereas the miR-204-5p expression was downregulated; miR-204-5p had a negative correlation with DNM3OS and HIP1, respectively, while DNM3OS and HIP1 were positively correlated with each other.
Conclusion:
Long non-coding RNA DNM3OS, miR-204-5p, and HIP1 form an axis that modulates oral cancer cell viability and migration.
Insights
Long non-coding RNA DNM3OS promotes oral cancer by targeting miR-204-5p and HIP1. Inhibiting DNM3OS or its axis may offer new oral cancer treatments.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Non-coding RNAs are crucial in oral cancer development.
- Identifying novel therapeutic targets is essential for oral cancer treatment.
Purpose of the Study:
- To identify long non-coding RNAs (lncRNAs) as potential therapeutic targets in oral cancer.
- To elucidate the underlying molecular mechanisms of identified lncRNAs in oral cancer.
Main Methods:
- Microarray profiling and RNA-sequencing identified lncRNA DNM3OS.
- DNM3OS knockdown and miRNA overexpression were performed in oral cancer cell lines.
- Targeted mRNA and miRNA interactions were verified experimentally.
Main Results:
- DNM3OS was upregulated in oral cancer tissues and cells, promoting cell viability and migration.
- DNM3OS targets miR-204-5p, which in turn targets HIP1, inhibiting oral cancer progression.
- A negative correlation was observed between miR-204-5p and DNM3OS/HIP1, while DNM3OS and HIP1 were positively correlated.
Conclusions:
- The lncRNA DNM3OS, miR-204-5p, and HIP1 form a regulatory axis.
- This axis significantly modulates oral cancer cell viability and migration.
- The DNM3OS/miR-204-5p/HIP1 axis represents a potential therapeutic target for oral cancer.
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