Patients with distant metastasis had significantly higher expression levels of microRNA-183 and microRNA-141 than patients without distant metastasis (p<0.01).
In addition, SNHG15 presented a downside tendency on regulating miR-141, and the miR-141 inhibitor dramatically changeover the impacts of SNHG15 depression on tumor growth and metastasis.
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 results suggest that miR-141 functions as a tumor suppressor in HNSCC and that it suppresses tumor growth and metastasis by suppressing EGFR signaling.
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).
Taken together, these data not only demonstrate an anti-angiogenic effect of miR-141, further strengthening the critical role of miR-200 family in the process of angiogenesis, but also provides a valuable cancer therapeutic target to control both angiogenesis and EMT, two essential steps in tumor growth and metastasis.
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.
In addition, decreased miR-141-3p levels were detected in the multiple tumor nodes group ( P = .004), the metastasis group ( P < .001), and the advanced TNM stage group ( P = .01), compared to the single tumor nodes group, the nonmetastasis group, and the early TNM stage group.
Clinically, prostate cancer (PCa) exhibits a high avidity to metastasize to bone. miR-141-3p is an extensively studied miRNA in cancers and downregulation of miR-141-3p has been widely reported to be involved in the progression and metastasis of several human cancer types.
Levels of miR-200c and miR-141 were lower in Foxp3 <sup>sf/+</sup> tumor cells than in normal breast epithelial cells, but plasma levels of miR-200c and miR-141 in the Foxp3 <sup>sf/+</sup> mice increased during tumor progression and metastasis.
MiR-200b, miR-200c, and miR-141 have been confirmed to be related to tumor metastasis. miR-141 levels in serum from experimental group was higher significant compared to control group (p = 0.024). miR-200b levels in serum from experimental group was significantly increased compared to control group (p = 0.031).
In this study, we performed a series of experiments <i>in vivo</i> and <i>in vitro</i> to determine whether exosomal miR-141-3p from MDA PCa 2b cells regulates osteoblast activity to promote osteoblastic metastasis.
In conclusion, miR-141 can be considered an important cancer suppressor gene of renal cancer by inhibiting proliferation and metastasis of renal cancer cells.