Correlation the between the regulation of miRNA-1 in c-Met-induced EMT and cervical cancer progression

Oncol Lett. 2019 Mar;17(3):3341-3349. doi: 10.3892/ol.2019.9971. Epub 2019 Jan 25.


Cervical cancer is a common malignant tumor of the female reproductive system. Despite advances in cervical cancer therapy, tumor recurrence and metastasis remain the leading cause of mortality for patients with cervical cancer. Therefore, the investigation of tumorigenesis and progression, and the search for novel therapeutic targets, has been the primary focus in cervical cancer research. The aims of the present study were: i) To analyze the alterations in c-Met, E-cadherin and microRNA (miRNA)-1 expression levels in cervical cancer tissues; ii) to assess the correlation between the above genes and the pathological characteristics of the cancer tissues; and iii) to examine the potential mechanism through which miRNA-1 may regulate c-Met-induced epithelial-mesenchymal transition to promote the development of cervical cancer. In cervical cancer tissues, c-Met was more highly expressed, while E-cadherin exhibited lower expression levels compared with the adjacent tissues. The 24-month follow-up reported that a lower c-Met expression level was correlated with higher E-cadherin expression levels and a longer survival rate. The miRNA-1 expression level in cancer tissues was 0.41±0.07 times lower compared with the adjacent tissues (P<0.01). A low miRNA expression level was correlated with a low survival rate of patients. In vitro, miRNA-1 inhibited the proliferation and migration of cervical cancer cell lines by downregulating c-Met mRNA. When miRNA-1 expression was downregulated in cervical cancer tissues, the inhibition of c-Met expression was reversed. The upregulation of c-Met expression levels was able to inhibit E-cadherin expression, which triggered the proliferation, migration and infiltration of cancer cells, and thus reduced patient survival rates.

Keywords: E-cadherin; c-Met; cervical cancer; microRNA-1; survival analysis.