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Updated: Feb 5, 2026

Modeling Oral-Esophageal Squamous Cell Carcinoma in 3D Organoids
Published on: December 23, 2022
miR-182-5p Promotes Growth in Oral Squamous Cell Carcinoma by Inhibiting CAMK2N1
Nan Li1, Chuan-Chuan Nan2, Xue-Yun Zhong3
1Department of Stomatology Center, Shenzhen People's Hospital, Second Clinical Medical School of Jinan University, Shenzhen, China.
Background/Aims:
Emerging evidence suggests that the propagation of oral squamous cell carcinoma (OSCC) is influenced by the abnormal expression of microRNAs (miRNAs). This study aimed to characterize the involvement of miR-182-5p in OSCC by targeting the calcium/ calmodulin-dependent protein kinase II inhibitor CAMK2N1.
Methods:
miR-182-5p expression was quantified in OSCC tissues and cell lines with reverse transcription polymerase chain reaction (RT-PCR). Cell colony formation, Cell Counting Kit-8 (CCK-8), Ki-67, and nude mouse xenograft assays were used to characterize the role of miR-182-5p in the proliferation of OSCC. A miR-182-5p target gene was identified with western blotting, RT-PCR, and luciferase activity assays. OSCC patient survival based on CAMK2N1 expression was also analyzed.
Results:
miR-182-5p was up-regulated in in vitro cell lines and in vivo clinical OSCC samples. CCK-8, colony formation, and Ki-67 assays revealed that miR-182-5p promoted the growth and proliferation of OSCC cells. miR-182-5p directly targeted CAMK2N1, as evidenced by luciferase assays and target prediction algorithms. CAMK2N1 operated as a tumor suppressor gene in patients with OSCC. Down-regulating miR-182-5p expression in the CAL-27 cell line restored CAMK2N1-mediated OSCC cell proliferation. miR-182-5p expression inhibited the activation of AKT, ERK1/2, and NF-κB. Mice injected with CAL-27 cells transfected with miR-182-5p-inhibitor demonstrated a significant increase in tumor size and weight and increased CAMK2N1 mRNA and protein expression compared with the miR-negative control group.
Conclusion:
The miR-182-5p-CAMK2N1 pathway can be potentially targeted to regulate the proliferation of OSCC cells.
Insights
MicroRNA-182-5p promotes oral squamous cell carcinoma (OSCC) growth by inhibiting the tumor suppressor CAMK2N1. Targeting this miR-182-5p-CAMK2N1 pathway offers a potential therapeutic strategy for OSCC proliferation.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Oral squamous cell carcinoma (OSCC) progression is linked to aberrant microRNA (miRNA) expression.
- MiRNAs play crucial roles in regulating cellular processes relevant to cancer development.
Purpose of the Study:
- To investigate the role of miR-182-5p in OSCC.
- To identify the downstream target of miR-182-5p in OSCC.
- To explore the therapeutic potential of targeting the miR-182-5p pathway in OSCC.
Main Methods:
- Quantification of miR-182-5p expression in OSCC tissues and cell lines using RT-PCR.
- Assessment of OSCC cell proliferation via colony formation, CCK-8, Ki-67 assays, and nude mouse xenografts.
- Identification of miR-182-5p targets using western blotting, RT-PCR, and luciferase assays.
- Analysis of patient survival in relation to CAMK2N1 expression.
Main Results:
- miR-182-5p was significantly upregulated in OSCC samples and promoted OSCC cell proliferation and growth.
- miR-182-5p directly targets CAMK2N1, which acts as a tumor suppressor in OSCC.
- Downregulation of miR-182-5p restored CAMK2N1 expression and suppressed OSCC cell proliferation.
- miR-182-5p inhibited the activation of key signaling pathways including AKT, ERK1/2, and NF-κB.
Conclusions:
- The miR-182-5p-CAMK2N1 axis is a critical regulator of OSCC cell proliferation.
- Targeting the miR-182-5p-CAMK2N1 pathway presents a promising therapeutic strategy for oral squamous cell carcinoma.
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