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Background  Cervical cancer is the leading cause of cancer-related death in women worldwide. However, the mechanisms mediating the development and progression of cervical cancer are unclear. In this study, we aimed to elucidate the roles of microRNAs and a1-chimaerin (CHN1) protein in cervical cancer progression.    Methods  The expression of  miR-205  and CHN1 protein was investigated by in situ hybridisation and immunohistochemistry. We predicted the target genes of  miR-205  using software prediction and dual luciferase assays. The expression of mRNAs and proteins was tested by qRT-PCR and western blotting respectively. The ability of cell growth, migration and invasion was evaluated by CCK-8 and transwell. Cell apoptosis was analysed by flow cytometry analysis.    Results  We found that  miR-205  and CHN1 were highly expressed in human cervical cancer tissue compared with paired normal cervical tissues. The  CHN1  gene was shown to be targeted by  miR-205  in HeLa cells. Interestingly, transfection with  miR-205  mimic upregulated CHN1 mRNA and protein, while  miR-205  inhibitor downregulated CHN1 in high-risk and human papilloma virus (HPV)-negative human cervical cancer cells in vitro,. These data suggested that  miR-205  positively regulated the expression of CHN1. Furthermore, the  miR-205  mimic promoted cell growth, apoptosis, migration, and invasion in high-risk and HPV-negative cervical cancer cells, while the  miR-205  inhibitor blocked these biological processes. Knockdown of CHN1 obviously reduced the aggressive cellular behaviours induced by upregulation of  miR-205 , suggesting that  miR-205  positively regulated CHN1 to mediate these cell behaviours during the development of cervical cancer. Furthermore, CHN1 was correlated with lymph node metastasis in clinical specimens.    Conclusions  Our findings showed that  miR-205  positively regulated CHN1 to mediate cell growth, apoptosis, migration, and invasion during cervical cancer development, particularly for high-risk HPV-type cervical cancer. These findings suggested that dysregulation of  miR-205  and subsequent abnormalities in CHN1 expression promoted the oncogenic potential of human cervical cancer.

bmc cancer

Upregulation of miR-205 induces CHN1 expression, which is associated with the aggressive behaviour of cervical cancer cells and correlated with lymph node metastasis