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Expression and prognostic value of Ars2 in hepatocellular carcinoma
Background Hepatocellular carcinoma (HCC) is one of the most common malignant tumors in China. Arsenic resistance protein 2 (Asr2) was reported to be important for microRNA (miR) biogenesis, and its depletion could reduce the levels of several miRs, including miR-21, which is over-expressed in HCC....
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Published in: | International journal of clinical oncology 2014-10, Vol.19 (5), p.880-888 |
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Main Authors: | , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Background
Hepatocellular carcinoma (HCC) is one of the most common malignant tumors in China. Arsenic resistance protein 2 (Asr2) was reported to be important for microRNA (miR) biogenesis, and its depletion could reduce the levels of several miRs, including miR-21, which is over-expressed in HCC. We hypothesized that Ars2 is also overexpressed in HCC and may be involved in the biological properties of HCC.
Methods
Ars2 immunolabeling was evaluated in 132 HCCs. Ars2 immunolabeling, Ars2 qRT-PCR and miR-21 were evaluated in 20 HCCs and in paired normal tissues. Ars2 shRNA was transfected into SMCC-7721 and HepG2 HCC cells. The cell proliferation and expression of Ars2 and miR-21 were subsequently evaluated.
Results
Ars2 was expressed primarily in the nucleus of HCC cells. The expression of Ars2 was statistically correlated with the loss of HCC differentiation and pathological stage. The survival rates of patients with low Ars2 expression in HCC were statistically higher than patients with overexpressed Ars2 in HCC. Ars2 and miR-21 were more highly expressed in HCC specimens than normal tissues, and they were also correlated. The knockdown of Ars2 in HCC cells inhibited miR-21 expression and cell proliferation.
Conclusions
Ars2 is overexpressed in HCC and may have prognostic value; it might play an important role in HCC proliferation and miR-21 expression. |
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ISSN: | 1341-9625 1437-7772 |
DOI: | 10.1007/s10147-013-0642-6 |