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Updated: Sep 1, 2025

Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis
Published on: March 30, 2019
MiR-222 regulates the progression of oral squamous cell carcinoma by targeting CDKN1B
Qun Chen1, Wenjuan Wang2, Yali Wang1
1Department of Endodontics, Hu'nan Xiangya Stomatological Hospital, Central South University Changsha 410000, Hu'nan Province, China.
Objective:
The purpose of this study was to establish a causal relationship between microRNA (miR-222) and oral squamous cell carcinoma (OSCC).
Methods:
The cell viability of each treatment group was measured by MTT. The effects of miR-222 on cell metastasis and apoptosis were measured by transwell and flow cytometry. The targeting relationship between miR-222 and CDKN1B was verified by dual-luciferase reporter gene assay and Western blot. Cell derived xenograft was further constructed to verify the effect of miR-222 on tumor growth by observing tumor weight and volume. The proliferation of tumor tissue was determined by hematoxylin-eosin staining and immunohistochemical staining.
Results:
Compared with those in adjacent tissues and normal cells, the levels of miR-222 in OSCC tissues and cells were significantly increased (P<0.05). The miR-222 mimic group promoted tumor cell proliferation, migration and cell cycle and inhibited cell apoptosis significantly (P<0.05). The up-regulation of CDKN1B expression inhibited cell viability, migration and invasiveness and promoted the apoptosis of OSCC (P<0.05). The dual-luciferase reporter gene assay found that miR-222 was targeted to CDKN1B and could inhibit fluorescence activity (P<0.05). In vivo assays showed that miR-222 could promote tumor growth through CDKN1B (P<0.05).
Conclusion:
MiR-222 was significantly upregulated in OSCC tissues and cells and regulated tumor progression by targeting CDKN1B.
Insights
MicroRNA 222 (miR-222) is elevated in oral squamous cell carcinoma (OSCC), promoting tumor growth by targeting CDKN1B. This study establishes a causal link between miR-222 and OSCC progression.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Oral squamous cell carcinoma (OSCC) is a prevalent malignancy.
- MicroRNAs (miRNAs) play critical roles in cancer development.
- The specific role of miR-222 in OSCC remains to be fully elucidated.
Purpose of the Study:
- To investigate the causal relationship between microRNA 222 (miR-222) and oral squamous cell carcinoma (OSCC).
- To explore the regulatory mechanism of miR-222 in OSCC progression.
Main Methods:
- Cell viability was assessed using MTT assays.
- Cell migration and apoptosis were measured by Transwell and flow cytometry.
- The interaction between miR-222 and CDKN1B was confirmed via dual-luciferase reporter gene assays and Western blot.
- Tumor growth was evaluated in vivo using xenograft models.
Main Results:
- miR-222 levels were significantly increased in OSCC tissues and cells compared to normal controls.
- Overexpression of miR-222 promoted OSCC cell proliferation, migration, and cell cycle progression while inhibiting apoptosis.
- CDKN1B upregulation suppressed OSCC cell viability, migration, and invasiveness, and induced apoptosis.
- miR-222 directly targets and inhibits CDKN1B, promoting tumor growth in vivo.
Conclusions:
- MiR-222 is significantly upregulated in OSCC.
- MiR-222 promotes OSCC progression by targeting and downregulating CDKN1B.
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