| Literature DB >> 27571925 |
Chaoxia Zou1, Chendan Zou1, Wanpeng Cheng1, Qiang Li2, Zhongjing Han3, Xiaona Wang1, Jianfeng Jin1, Jiaqi Zou4, Zhiyan Liu4, Zhongqiu Zhou4, Weiming Zhao1, Zhimin Du4.
Abstract
Heme metabolism system is involved in microRNA (miRNA) biogenesis. The complicated interplay between heme oxygenase-1 (HO-1) and miRNA has been observed in various tissues and diseases, including human malignancy. In the present study, our data showed that stable HO-1 overexpression in hepatocellular carcinoma (HCC) cells downregulated several oncomiRs. The most stably downregulated are miR-30d and miR-107. Iron, one of HO-1 catalytic products, was an important mediator in this regulation. Cell function analysis demonstrated that HO-1 inhibited the proliferation and metastasis of HepG2 cells, whereas miR-30d/miR-107 improved the proliferative and migratory ability of HepG2 cells. The beneficial effect of HO-1 in HCC inhibition could be reversed by upregulating miR-30d and miR-107. Akt and ERK pathways may be involved in the regulation of HO-1/miR-30d/miR-107 in HCC. These data indicate that HO-1 significantly suppresses HCC progression by regulating the miR-30d/miR-107 level, suggesting miR-30d/miR-107 regulation as a new molecular mechanism of HO-1 anticancer effect.Entities:
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Year: 2016 PMID： 27571925 DOI： 10.3892/or.2016.5056
Source DB: PubMed Journal: Oncol Rep ISSN： 1021-335X Impact factor: 3.906