MiR-30c-5p suppresses migration, invasion and epithelial to mesenchymal transition of gastric cancer via targeting MTA1.

In China, gastric cancer (GC) is an ordinary malignant tumor. Recent literatures have shown that microRNA is critical during tumorigenesis. This study focuses on the influence of miR-30c-5p on the metastasis of GC and further explores its underlying mechanism. Before the study, expression level of miR-30c-5p and targeted protein was detected in 40 GC tissue samples and 5 GC cells by RT-qPCR. Meanwhile, correlation analysis was conducted between miR-30c-5p expression level and clinicopathological features. In addition, wound healing assay and cell invasion assay were utilized to identify whether miR-30c-5p could affect the migrated and invaded ability of GC cells. Western blotting assay and luciferase assay were used to explore the potential mechanism. In GC tissues, miR-30c-5p expression level was significantly lower and was remarkably related with clinical features such as tumor node metastasis(TNM) stage and lymphatic metastasis. Moreover, the migrated and invaded ability of GC cells was enhanced through knockdown of miR-30c-5p, while overexpression of miR-30c-5p presented with reversed effect. Further study showed that miR-30c-5p inhibited the expression of its target spot, metastasis-associated protein 1(MTA1), and then suppressed the process of epithelial to mesenchymal transition(EMT) which was important in the metastasis of GC. The results indicate that miR-30c-5p, a novel suppressor in tumorigenesis, could inhibit the metastasis and EMT via MTA1, which may offer a possible therapeutic target in GC.

Cao JM ，Li GZ ，Han M ，Xu HL ，Huang KM ... -  《-》

sMicroRNA-28-5p acts as a metastasis suppressor in gastric cancer by targeting Nrf2.

The transcription factor nuclear factor (erythroid-2)-related factor 2 (Nrf2) can principally serve a mode of protection for both the normal cells and cancer cells from cellular stress, and elevates cancer cell survival. microRNA-28 (miR-28) has been involved in the regulation of Nrf2 expression in breast epithelial cells. However, no comprehensive analysis has been conducted regarding the function of miR-28-5p regulating Nrf2 in gastric cancer (GC). In this study, we aimed to evaluate their interaction and biological roles in the migration and invasion of GC cells. The expression of Nrf2 in the cancer tissues harvested from 42 patients with GC was examined by an array of molecular techniques comprising of Immunohistochemical staining, RT-qPCR and Western blot analysis. Kaplan-Meier method was adopted for analysis of the correlation of Nrf2 with the prognosis of GC patients. Interaction between miR-28-5p and Nrf2 was determined using the bioinformatics analysis and dual luciferase reporter gene assay. Gain- and loss-of-function studies of miR-28-5p and Nrf2 were conducted to elucidate their effects on GC cell migration, invasion and metastasis, as well as expression pattern of several epithelial-mesenchymal transition (EMT)-related proteins. Results indicated that the expression pattern of Nrf2 was significantly upregulated in GC tissues and indicative of poor prognosis of GC patients. miR-28-5p was verified to target Nrf2 and downregulate its expression. GC cells with overexpression of miR-28-5p or Nrf2 knockdown exhibited a marked reduction in the migrated and invasive abilities, along with the N-cadherin expression yet an increase of E-cadherin expression. Furthermore, miR-28-5p exerted an inhibitory function on the metastatic and tumorigenicity of GC cells. In conclusion, miR-28-5p is a comprehensive tumor suppressor that inhibits GC cell migration and invasion through repressing the Nrf2 expression. Therefore, miR-28-5p may serve as a potential biomarker for the prognosis of GC and a novel therapeutic target in advanced GC.

Yue CF ，Li LS ，Ai L ，Deng JK ，Guo YM ... -  《-》

MicroRNA-30c inhibits metastasis of ovarian cancer by targeting metastasis-associated gene 1.

Wang X ，Qiu LW ，Peng C ，Zhong SP ，Ye L ，Wang D ... -  《-》

microRNA-30c negatively regulates endometrial cancer cells by targeting metastasis-associated gene-1.

Zhou H ，Xu X ，Xun Q ，Yu D ，Ling J ，Guo F ，Yan Y ，Shi J ，Hu Y ... -  《-》

Effects of microRNA-183 on epithelial-mesenchymal transition, proliferation, migration, invasion and apoptosis in human pancreatic cancer SW1900 cells by targeting MTA1.

This study aims to explore effects of miR-183 on epithelial-mesenchymal transition (EMT) and invasion by targeting MTA1 in human pancreatic cancer (PC) cells. Totally, 108 PC patients admitted in Wenzhou Central Hospital and Wenzhou People's Hospital, The Dingli Clinical Institute of Wenzhou Medical University from March 2010 to March 2014 were enrolled. qRT-PCR and immunohistochemistry were applied to examine expression of MTA1 mRNA and protein. Samples were divided into 6 groups: blank, NC, miR-183 mimics, miR-183 inhibitors, MTA1-siRNA and miR-183 inhibitors +MTA1-siRNA groups. CCK8 method was employed for determining cell proliferation rate, flow cytometry for cell apoptosis rate, scratch test for cell migration and Transwell assay for cell invasion. qRT-PCR and Western blotting were used to determine expression of MTA1, E-cadherin and Vimentin mRNA and protein. Positive expression rate of MTA1 was upregulated in PC tissues, and expression of miR-183 and MTA1 was associated with differentiation, migration, tumor size, TNM. The miR-183 mimics and MTA1-siRNA groups showed a decrease in proliferation, migration and invasion, whereas increased apoptosis, in comparison with blank and NC groups, as expression of MTA1 and Vimentin mRNA and protein were reduced, expression of E-cadherin mRNA and protein was elevated. Compared to blank and NC groups, the miR-183 inhibitors group exhibited enhanced proliferation, migration and invasion and inhibited apoptosis; increased expressions of MTA1 and Vimentin mRNA and protein and decreased expressions of E-cadherin mRNA and protein. Our study supported that miR-183 could repress EMT and invasion of human PC cells through inhibition of MTA1 expression.

Lin X ，Zheng L ，Song H ，Xiao J ，Pan B ，Chen H ，Jin X ，Yu H ... -  《-》