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miR-372 down-regulates the oncogene ATAD2 to influence hepatocellular carcinoma proliferation and metastasis.

Wu G, Liu H, He H, Wang Y, Lu X, Yu Y, Xia S, Meng X, Liu Y - BMC Cancer (2014)

Bottom Line: In addition, ATAD2 knockdown was found to extremely up-regulate APC expression and down-regulate CTNNA1 at the mRNA level.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.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of General Surgery, the First Affiliated Hospital of China Medical University, Shenyang, Liaoning 110001, China. wugang@mail.cmu.edu.cn.

ABSTRACT

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.

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Related in: MedlinePlus

Transwell assays of Huh7 and HCCLM3 cells transfected with control and ATAD2 siRNA. (a). ATAD2 depletion had a measurable inhibitory effect on cell invasion in both cell lines. (b). The numbers of invading cells were counted, and a significant difference was observed (*P < 0.05). (c). A significant difference was observed in both cell lines and (d) the numbers of migrating cells were counted (*P < 0.05).
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Figure 5: Transwell assays of Huh7 and HCCLM3 cells transfected with control and ATAD2 siRNA. (a). ATAD2 depletion had a measurable inhibitory effect on cell invasion in both cell lines. (b). The numbers of invading cells were counted, and a significant difference was observed (*P < 0.05). (c). A significant difference was observed in both cell lines and (d) the numbers of migrating cells were counted (*P < 0.05).

Mentions: Cell invasion and migration assays demonstrated that the Huh7 and HCCLM3 liver cancer cell lines that were transfected with ATAD2 siRNA displayed more attenuated invasive and migratory capacities than those of the negative controls (Figure 5).


miR-372 down-regulates the oncogene ATAD2 to influence hepatocellular carcinoma proliferation and metastasis.

Wu G, Liu H, He H, Wang Y, Lu X, Yu Y, Xia S, Meng X, Liu Y - BMC Cancer (2014)

Transwell assays of Huh7 and HCCLM3 cells transfected with control and ATAD2 siRNA. (a). ATAD2 depletion had a measurable inhibitory effect on cell invasion in both cell lines. (b). The numbers of invading cells were counted, and a significant difference was observed (*P < 0.05). (c). A significant difference was observed in both cell lines and (d) the numbers of migrating cells were counted (*P < 0.05).
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4016509&req=5

Figure 5: Transwell assays of Huh7 and HCCLM3 cells transfected with control and ATAD2 siRNA. (a). ATAD2 depletion had a measurable inhibitory effect on cell invasion in both cell lines. (b). The numbers of invading cells were counted, and a significant difference was observed (*P < 0.05). (c). A significant difference was observed in both cell lines and (d) the numbers of migrating cells were counted (*P < 0.05).
Mentions: Cell invasion and migration assays demonstrated that the Huh7 and HCCLM3 liver cancer cell lines that were transfected with ATAD2 siRNA displayed more attenuated invasive and migratory capacities than those of the negative controls (Figure 5).

Bottom Line: In addition, ATAD2 knockdown was found to extremely up-regulate APC expression and down-regulate CTNNA1 at the mRNA level.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.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of General Surgery, the First Affiliated Hospital of China Medical University, Shenyang, Liaoning 110001, China. wugang@mail.cmu.edu.cn.

ABSTRACT

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.

Show MeSH
Related in: MedlinePlus