The restoration of miR-203 in highly metastatic breast cancer cells inhibited tumor cell invasion in vitro and lung metastatic colonization in vivo by repressing SNAI2.
Here, co-transfection of miR-203-3p mimics and miR-21-5p inhibitors led to an extraordinary increased expression of miR-203-3p and synergistically inhibited proliferation, migration, and invasion in EC cells.
In contrast, miR-203 was mainly expressed in tumours exhibiting the characteristics associated with a good prognosis, was mainly present in well-differentiated zones, and rarely expressed in the invasion front.
Overexpression of miR-203 inhibits EMT by targeting BIRC5 in ovarian cancer SKOV3 and OVCAR3 cells. miR-203 expression enhances the ability of the survivin inhibitor YM155 to reduce tumor cell migration and invasion in vitro.
To understand the role of miRNAs in Regulator of G Protein Signaling 17 (RGS17)-induced NSCLC, we showed that miR-203 was downregulated during tumorigenesis, and inhibited the proliferation and invasion of lung cancer cells.
We showed here that overexpression of miR-203 in esophageal cancer cells dramatically increased cell apoptosis and inhibited cell proliferation, migration and invasion as well as tumor growth and down-regulated miR-21 expression.
The expression of miR-203 is downregulated in lung cancer cells. miR-203 negatively regulates survivin protein expression and inhibits the proliferation and invasion of lung cancer cells.
The miR-203 expression was detected by qRT-PCR; The cell viability was measured by MTT assay; The cell proliferation was measured by BrdU assay; The cell invasion was measured by Transwell assay; The protein expression was detected by Western blot; The target relationship between miR-203 and mRNA was measured by dual-luciferase assay.
The overexpression of miR‑203a‑3p was shown to inhibit the invasion and migration of human CRC SW480 and HT29 cells, and increase their apoptosis rates.
The expression level of messenger RNA and matrix metalloproteinase-9 to assess cell invasion and the expression level of miR-203, miR-145, and CXCR4 receptor were measured by quantitative real-time polymerase chain reaction analysis on the MDA-MB-468 cell lines.
In vitro experiments revealed that miR‑203 overexpression significantly downregulated VEGFA expression and inhibited the proliferation, migration and invasion ability of HTR‑8/SVneo cells.