miR-224-3p inhibits autophagy in cervical cancer cells by targeting FIP200

• DOI: 10.1038/srep33229
• Publication Date: 2016-09-12T11:26:29Z
• Authors: Wang Fang; Shan Shu; Li Yongmei; Zhu Endong; Yin Lirong; Sun Bei
• Keywords: 0303 health sciences; Binding Sites; Base Sequence; Papillomavirus Infections; Autophagy-Related Proteins; Gene Expression; Uterine Cervical Neoplasms; Protein-Tyrosine Kinases; Article; 3. Good health; Gene Expression Regulation, Neoplastic; MicroRNAs; 03 medical and health sciences; Autophagy; Humans; Female; RNA Interference; 3' Untranslated Regions; HeLa Cells

AbstractCervical cancer (CC) is a malignant solid tumor, which is one of the main causes of morbidity and mortality in women. Persistent High-risk human papillomavirus (hrHPV) infection is closely related to cervical cancer and autophagy has been suggested to inhibit viral infections. miRNAs have been reported to regulate autophagy in many solid tumors with many studies implicating miR-224-3p in the regulation of autophagy. In this study, we performed a miRNA microarray analysis on CC tissues and found that a large number of miRNAs with differential expressions in hrHPV-infected tissues. We identified miR-224-3p as a candidate miRNA selectively up regulated in HPV-infected tissues and cell lines. Further analysis revealed that miR-224-3p regulates autophagy in cervical cancer tissues and cell lines. While the overexpression of miR-224-3p inhibits autophagy in HPV-infected cells, knocking down endogenous miR-224-3p increases autophagy activity in the same cells. In addition, we found that miR-224-3p directly inhibits the expression of autophagy related gene, FAK family-interacting protein of 200 kDa (FIP200). In summary, we found that miR-224-3p regulates autophagy in hrHPV-induced cervical cancer cells through targeting FIP200 expression.