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Updated: May 2, 2026

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
Published on: August 23, 2019
miR-372 down-regulates the oncogene ATAD2 to influence hepatocellular carcinoma proliferation and metastasis
1Department of General Surgery, the First Affiliated Hospital of China Medical University, Shenyang, Liaoning 110001, China. wugang@mail.cmu.edu.cn.
Background:
ATAD2 is associated with many cellular processes, such as cell growth, migration and invasion. However, no studies have been conducted on the molecular biological function of the ATAD2 gene in hepatocellular carcinoma (HCC).
Methods:
The protein and mRNA level expression of ATAD2 was examined in tissues and cell lines. Prognostic significance was analyzed by the Kaplan-Meier survival method and Cox regression. ATAD2 knockdown was used to analyze cell proliferation and invasion. The upstream and downstream of ATAD2 was analyzed by RT2 Profiler™ PCR array and luciferasex fluorescence system.
Results:
ATAD2 was highly expressed in liver cancer samples and correlated with poor survival. High ATAD2 expression was positively correlated with metastasis (P = 0.005) and was an independent prognostic factor in HCC (P = 0.001). ATAD2 depletion by RNA interference reduced their capacity for invasion and proliferation and led to a G1 phase arrest in vitro. Further study revealed that miR-372 was an upstream target of ATAD2 as miR-372 was bound directly to its 3' untranslated region (3' UTR). In addition, ATAD2 knockdown was found to extremely up-regulate APC expression and down-regulate CTNNA1 at the mRNA level.
Conclusions:
The findings demonstrated that miR-372 suppressed the expression of ATAD2, which was highly expressed in HCC and exerted a proto-oncogene effect in hepatic carcinogenesis. In conclusion, ATAD2 may promote HCC progression.
Insights
The ATAD2 gene is highly expressed in hepatocellular carcinoma (HCC), promoting cancer progression and metastasis. Inhibiting ATAD2 may offer a therapeutic strategy for liver cancer.
Area of Science:
- Molecular biology
- Oncology
- Hepatocellular Carcinoma Research
Background:
- The role of ATAD2 in hepatocellular carcinoma (HCC) remains uninvestigated.
- ATAD2 is implicated in cellular processes including growth, migration, and invasion.
Purpose of the Study:
- To investigate the molecular biological function of the ATAD2 gene in HCC.
- To determine the prognostic significance of ATAD2 in HCC patients.
Main Methods:
- Examined ATAD2 protein and mRNA expression in HCC tissues and cell lines.
- Utilized Kaplan-Meier survival analysis and Cox regression for prognostic significance.
- Performed ATAD2 knockdown via RNA interference to assess effects on proliferation and invasion.
- Analyzed upstream and downstream targets using RT2 Profiler™ PCR array and luciferase assays.
Main Results:
- ATAD2 was highly expressed in HCC tissues and correlated with poor patient survival.
- High ATAD2 expression was linked to metastasis and served as an independent prognostic factor for HCC.
- ATAD2 depletion reduced HCC cell invasion and proliferation, causing G1 phase arrest.
- miR-372 was identified as an upstream regulator, directly binding to the 3' UTR of ATAD2.
- ATAD2 knockdown significantly upregulated APC and downregulated CTNNA1 mRNA levels.
Conclusions:
- miR-372 suppresses ATAD2 expression in HCC.
- ATAD2 acts as a proto-oncogene in hepatic carcinogenesis, promoting HCC progression.
- ATAD2 is a potential therapeutic target for hepatocellular carcinoma.
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