LncRNA PVT1 was overexpressed in bladder cancer cells, and it was downregulated miR-31 to enhance CDK1 expression and facilitate bladder cancer cells proliferation, migration, and invasion.
Compared with those in the negative control group, the proliferation and invasion abilities of cells transfected with miR-31 mimics were notably enhanced (p < 0.01), and those of cells transfected with anti-miR-31 were significantly reduced (p < 0.01).
The aim of this study was to investigate the effect of miR-31 and miR-143 inhibition on metastasis and invasion in both MDA-MB231, MDA-MB468 as well as the MCF-7 breast cancer cell lines and 5-week old female mice.
In the present study, the consequences of co-transfecting breast cancer cell lines with miR-193b and miR-31 were investigated via invasion and migration assays.
Induction of miR-31 in MKN-45 followed by suppression of RhoA expression resulted in increased sensitivity to 5-fluorouracil, inhibition of cell proliferation, and invasion compared to the control groups.
Moreover, the decreased expression of miR-31 was demonstrated to be associated with lymph node metastasis, poor pT and pN stage, and invasion ability into lymphatic vessels as determined by the Mann-Whitney U test.
In summary, our study demonstrates that the suppressive effect of miR-31 on glioma cell migration and invasion is p21-dependent, and suggests that miR-31 may be used for the treatment of patients with p21-deficent glioma.
Ectopic overexpression of miR-31 decreased cell proliferation, viability and invasion capacity, but promoted apoptosis in DDP-resistant cells and in xenograft tumor models.
Ectopic expression of miR-31 reduced tumor cell viability, enhanced apoptosis, arrested tumor cells at G1 transition, and reduced tumor cell migration and invasion in SGC-7901 and MGC-803 gastric cell lines in vitro.
Oncogenic KRAS can activate Rho through the miR-31-mediated regulation of RASA1 indicating miR-31 acts as a KRAS effector to modulate invasion and migration in pancreatic cancer.
MiR-31 expression was increased after MDA-MB-231 cell was treated by 5-aza-2'-deoxycytidine (5-AZA-CdR), enhance the expression of miR-31 significantly inhibited MDA-MB-231 cell migration and invasion, downregulation of miR-31 expression could promoted MCF-7 cell migration and invasion.
CONCLUSIONS We found miR-31 could downregulate the ROCK/MLC pathway by inhibiting the expression of RhoA in order to suppress the invasion and migration of GC cells.