Overexpressed miR-141-3p in HTR-8/SVneo cells contributed to increased cell proliferation, invasion, and migration. miR-141-3p inhibition in HTR-8/SVneo cells resulted in decreased cell proliferation and invasion.
Our data show that forced expression of miR-141 or miR-200c suppressed invasion and metastasis of PDAC cells both in vitro and in xenograft and identified WIPF1 as a direct target of miR-141 and miR-200c.
MiR-141 promoted the proliferation and invasion by targeting the KLF9 in non-small cell lung cancer, and the newly identified miR-141/KLF9 axis provides novel insight into the pathogenesis of non-small cell lung cancer.
Elevated miR-141 and miR-200a inhibited the expression of EG-VEGF, downstream extracellular signal-regulated kinase (ERK)/matrix metalloproteinase 9 signalling and cilia formation, thus leading to defective trophoblast invasion.
Further gain-of-function and loss-of-function analysis revealed that miR-141 not only limited the migration and invasion of the gastric cancer cells, but also inhibited the transition of NFs and BMSC to CAFs.
The effects of miR-141 mimics were investigated with respect to angiogenesis by vascular endothelial growth factor (VEGF), epithelial-mesenchymal transition (EMT) by E-cadherin, metastasis by Igfbp-4 and Tinagl1 enzyme-linked immunosorbent assays, invasion by an invasion chamber, and apoptosis by Annexin V.
These findings indicated that miR‑141 inhibited HCC cell proliferation and invasion by directly downregulating TGFβR1 and its downstream signaling cascade, providing insights into a potential novel strategy for HCC therapy.
The in vitro experiments showed that restoration of ZFR rescued the miR-141-3p-mediated inhibitory effects on cell proliferation, migration and invasion in NSCLC cells.
The miR-200 family, consisting of miR-200a/b/c, miR-141, and miR-429, is well known to inhibit epithelial-to-mesenchymal transition (EMT) in cancer invasion and metastasis.
Moreover, the expression levels of miR-182, miR-183, miR-141, and miR-21 were demonstrated to be associated with a gradual increase in fold change expression with depth of tumor invasion (all P < .05), lymph node invasion (all P < .001), and maximal increase with distant metastasis (all P < .001).
After down-regulation of EGFR by siRNA in CRC cells, the effects of miR-141-3p on proliferation, migration and invasion were reversed. miR-141-3p played important roles in CRC growth and response to cetuximab treatment, and might function as a potential biomarker to predict cetuximab response.