Cheng Yun, Yang Minliang, Peng Jingxian
Department of Histology and Embryology, School of Preclinical and Forensic Medicine, Baotou Medical College, Baotou, Inner Mongolia 014000, P.R. China.
Medical Ultrasound Center, Northwest Women's and Children's Hospital, Xian, Shanxi 710000, P.R. China.
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. , 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.
宫颈癌是女性生殖系统常见的恶性肿瘤。尽管宫颈癌治疗取得了进展,但肿瘤复发和转移仍然是宫颈癌患者死亡的主要原因。因此,研究肿瘤发生和进展以及寻找新的治疗靶点一直是宫颈癌研究的主要重点。本研究的目的是:i)分析宫颈癌组织中c-Met、E-钙黏蛋白和微小RNA(miRNA)-1表达水平的变化;ii)评估上述基因与癌组织病理特征之间的相关性;iii)研究miRNA-1可能通过调控c-Met诱导的上皮-间质转化促进宫颈癌发展的潜在机制。与相邻组织相比,宫颈癌组织中c-Met表达更高,而E-钙黏蛋白表达水平更低。24个月的随访报告显示,较低的c-Met表达水平与较高的E-钙黏蛋白表达水平及较长的生存率相关。癌组织中miRNA-1表达水平比相邻组织低0.41±0.07倍(P<0.01)。低miRNA表达水平与患者低生存率相关。miRNA-1通过下调c-Met mRNA抑制宫颈癌细胞系的增殖和迁移。当宫颈癌组织中miRNA-1表达下调时,对c-Met表达的抑制作用被逆转。c-Met表达水平上调能够抑制E-钙黏蛋白表达,从而引发癌细胞的增殖、迁移和浸润,进而降低患者生存率。