miR-372 down-regulates the oncogene ATAD2 to influence hepatocellular carcinoma proliferation and metastasisReport as inadecuate

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BMC Cancer

, 14:107

Translational oncology


BackgroundATAD2 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.

MethodsThe 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 RT Profiler™ PCR array and luciferasex fluorescence system.

ResultsATAD2 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.

ConclusionsThe 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.

Electronic supplementary materialThe online version of this article doi:10.1186-1471-2407-14-107 contains supplementary material, which is available to authorized users.

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Author: Gang Wu - Haiyang Liu - Hui He - Yawei Wang - Xiaojun Lu - Yanqiu Yu - Shuguan Xia - Xiangyu Meng - Yongfeng Liu

Source: https://link.springer.com/


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