| First Author | He Q | Year | 2017 |
| Journal | Tumour Biol | Volume | 39 |
| Issue | 10 | Pages | 1010428317737729 |
| PubMed ID | 29072132 | Mgi Jnum | J:320948 |
| Mgi Id | MGI:6883406 | Doi | 10.1177/1010428317737729 |
| Citation | He Q, et al. (2017) Intravenous miR-144 inhibits tumor growth in diethylnitrosamine-induced hepatocellular carcinoma in mice. Tumour Biol 39(10):1010428317737729 |
| abstractText | Previous in vitro studies have demonstrated that miR-144 inhibits hepatocellular carcinoma cell proliferation, invasion, and migration. We have shown that miR-144, injected intravenously, is taken up by the liver and induces endogenous hepatic synthesis of miR-144. We hypothesized that administered miR-144 has tumor-suppressive effects on liver tumor development in vivo. The effects of miR-144 on tumorigenesis and tumor growth were tested in a diethylnitrosamine-induced hepatocellular carcinoma mouse model. MiR-144 injection had no effect on body weight but significantly reduced diethylnitrosamine-induced liver enlargement compared with scrambled microRNA. MiR-144 had no effect on diethylnitrosamine-induced liver tumor number but reduced the tumor size above 50%, as evaluated by magnetic resonance imaging (scrambled microRNA 23.07 +/- 5.67 vs miR-144 10.38 +/- 2.62, p < 0.05) and histological analysis (scrambled microRNA 30.75 +/- 5.41 vs miR-144 15.20 +/- 3.41, p < 0.05). The levels of miR-144 was suppressed in tumor tissue compared with non-tumor tissue in all treatment groups (diethylnitrosamine-phosphate-buffered saline non-tumor 1.05 +/- 0.09 vs tumor 0.54 +/- 0.08, p < 0.01; diethylnitrosamine-scrambled microRNA non-tumor 1.23 +/- 0.33 vs tumor 0.44 +/- 0.10, p < 0.05; diethylnitrosamine-miR-144 non-tumor 54.72 +/- 11.80 vs tumor 11.66 +/- 2.75, p < 0.01), but injection of miR-144 greatly increased miR-144 levels both in tumor and non-tumor tissues. Mechanistic studies showed that miR-144 targets epidermal growth factor receptor and inhibits the downstream Src/AKT signaling pathway which has previously been implicated in hepatocellular carcinoma tumorigenesis. Exogenously delivered miR-144 may be a therapeutic strategy to suppress tumor growth in hepatocellular carcinoma. |
