Yao Yang1, Hong Liu1, Xi Wang1, Long Chen1. 1. Department of Gynecology, Qingdao Municipal Hospital 1 Jiaozhou Road, Qingdao 266000, China.
Abstract
BACKGROUND: Cervical cancer is one of the leading causes of cancer-related death in woman worldwide. In the present study, we investigated the role of microRNA 664 (miR-664) in regulating cancer migration and chemotherapy sensitivity in cervical cancer. METHODS: Quantitative real-time PCR (qPCR) was used to assess the mRNA levels of miR-664 in both cervical cancer cell lines and cancer tissues from human patients. Lentiviral vector containing miR-664 mimics (lv-miR-664) was used to upregulate endogenous miR-664 in cervical cancer HeLa cells. The effects of miR-664 up-regulation on cervical cancer cell migration and cisplatin sensitivity were assessed by MTT and Cisplatin assays. Furthermore, the effect of miR-664 up-regulation on E-Cadherin expression was examined by western blot. E-Cadherin was then silenced by siRNA to examine its effect on miR-664 regulation on cervical cancer cell. RESULTS: MiR-664 was downregulated in both cervical cancer cell lines and cancer tissues in patients. In HeLa cells, lentivirus mediated miR-664 up-regulation reduced cancer cell migration and increased chemosensitivity to cisplatin. Western blot showed E-Cadherin was upregulated upon miR-664 overexpression in HeLa cells. Genetic silencing of E-Cadherin by siRNA reversed the inhibitory effect of miR-664 up-regulation on cervical cancer cell migration. CONCLUSION: Our study demonstrated that miR-664 played an important role in regulating cervical cancer, possibly modulated by E-Cadherin.
BACKGROUND:Cervical cancer is one of the leading causes of cancer-related death in woman worldwide. In the present study, we investigated the role of microRNA 664 (miR-664) in regulating cancer migration and chemotherapy sensitivity in cervical cancer. METHODS: Quantitative real-time PCR (qPCR) was used to assess the mRNA levels of miR-664 in both cervical cancer cell lines and cancer tissues from humanpatients. Lentiviral vector containing miR-664 mimics (lv-miR-664) was used to upregulate endogenous miR-664 in cervical cancer HeLa cells. The effects of miR-664 up-regulation on cervical cancer cell migration and cisplatin sensitivity were assessed by MTT and Cisplatin assays. Furthermore, the effect of miR-664 up-regulation on E-Cadherin expression was examined by western blot. E-Cadherin was then silenced by siRNA to examine its effect on miR-664 regulation on cervical cancer cell. RESULTS:MiR-664 was downregulated in both cervical cancer cell lines and cancer tissues in patients. In HeLa cells, lentivirus mediated miR-664 up-regulation reduced cancer cell migration and increased chemosensitivity to cisplatin. Western blot showed E-Cadherin was upregulated upon miR-664 overexpression in HeLa cells. Genetic silencing of E-Cadherin by siRNA reversed the inhibitory effect of miR-664 up-regulation on cervical cancer cell migration. CONCLUSION: Our study demonstrated that miR-664 played an important role in regulating cervical cancer, possibly modulated by E-Cadherin.
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