Abstract
Hepatocellular carcinoma (HCC) is a primary liver cancer with high incidence and mortality. miR-185, a microRNA with appriximately 22-28 nucleotides, was reported to be involved in many cancers. The potential mechanism of miR-185 on HCC through cell division cycle 42 (CDC42) was investigated. RT-qPCR was used to measure the RNA level of miR-185 and CDC42 in HCC tissues and cells. The dual luciferase reporter assay was used to verify whether CDC42 was a target gene for miR-185. Transwell assay was employed to detect the ability of migration and invasion to change miR-185. miR-185 expression was low in HCC and negatively correlated with CDC42. miR-185 inhibited HCC migration, invasion and miR-185 low expression predicted poor prognosis. CDC42 was predicted to be a target gene for miR-185, and regulated by miR-185. miR-185 suspressed the ability of cell migration and invasion through CDC42 in HCC. In conclusion, miR-185 suspressed migration and invasion of HCC cells by directly targeting CDC42. It is suggested that miR-185/CDC42 axis may present a novel target for HCC treatment.
Highlights
Primary liver cancer is a malignant tumor, incidence rate was the fifth and the mortality ranked third in 2007, and approximately 85-90% was hepatocellular carcinoma (HCC)
cell division cycle 42 (CDC42) was overexpressed in HCC cell lines HuH-7 vs. normal liver L-02 cells (P
The results showed that when interfered with CDC42, the cells number of migration and invasion was reduced in HuH-7 (P=0.0043 and 0.0002) cells, which illustrated that the interfered CDC42 expression could reverse the partial function of miR-185
Summary
Primary liver cancer is a malignant tumor, incidence rate was the fifth and the mortality ranked third in 2007, and approximately 85-90% was hepatocellular carcinoma (HCC). Identification of tumor biomarkers for early diagnosis is essential for HCC patients. MiR-185 was reported to play important roles in several human cancers, covering prostate carcinoma, lung cancer, ovarian, pediatric renal, breast, cervical and colon cancers [6,7,8,9,10]. MiR-185 downregulated androgen receptor (AR) to inhibit cell proliferation and induced apoptosis by directly targeting it [6]. MiR-185 inhibited colorectal cell proliferation by targeting RhoA and CDC42 [11] MiR-185 downregulated androgen receptor (AR) to inhibit cell proliferation and induced apoptosis by directly targeting it [6]. miR-185 inhibited colorectal cell proliferation by targeting RhoA and CDC42 [11]
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