Taken together, our study provided the first compelling evidence that ING4 can suppress human HCC growth and metastasis to a great extent via a NF-κB/miR-155/FOXO3a pathway.
Sevoflurane inhibited migration and invasion, while enhanced cell apoptosis by downregulating miR-155 in PTC cells, suggesting important clinical implications for anesthetic agents to prevent the metastasis in PTC.
The effect of miR-155-5p on cervical carcinoma cell growth and metastasis in vivo was investigated using xenograft model and experimental lung metastasis model.
Additionally, the downregulation of miR-155 expression in gastric carcinoma cell lines was able to significantly decrease the expression of VEGF, MMP2 and MMP9, thereby inhibiting the invasion and metastasis of gastric carcinoma cells.
The study indicated that transfection of miR-155-5p mimic significantly suppressed cell proliferation, migration and invasion of A549 cells, whereas its inhibition significantly promoted cell proliferation, migration and invasion of A549 cells, suggesting a potential therapeutic application of miR-155-5p in controlling lung cancer metastasis.
These results suggested that miR-155 prevented colorectal cancer progression and metastasis via silencing CTHRC1 <i>in vitro</i>, which provides evidence for miR-155 and CTHRC1 as a novel anti-onco molecular target for the treatment of colorectal cancer in the future.
The findings of this study suggest that miR-155 and β-catenin may have a unique potential as a novel biomarker candidate for diagnosis and treatment of tumor metastasis.
Additionally, miR-155-5p overexpression increased metastasis- and anti-apoptosis-related protein expression and decreased pro-apoptosis-related protein expression, while forced CTHRC1 expression conserved the expression of these proteins.
Taken together, these results show that miR-155-5p positively regulates RhoA mRNA levels and translation as well as cell migration in serum starved colon cancer cells and indicate that targeting miR-155-5p might be a useful strategy to antagonize colon cancer metastasis.
A vast number of miRNAs, including the well-studied miR-21, miR-155 and miR-34, has been shown to regulate PDAC growth, invasion and metastasis in vitro and in vivo by targeting members of key signaling pathways.
We found that miR-155 expression was markedly up-regulated in cervical cancer tissues and correlated with FIGO stage, lymph nodes metastasis, vascular invasion and HPV.
Expression of miR-9, miR-10b, miR-145, and miR-155, 4 miRNAs previously shown to play roles in metastasis in other tumor types, was compared in lymph node (LN)-positive NSCLC versus LN-negative NSCLC.
The miRNA microarray assay revealed miR-155 to be highly expressed and biologically active in chordoma. miR-155 expression in chordoma tissues was significantly elevated, and this expression correlated significantly with disease stage (p = 0.036) and the presence of metastasis (p = 0.035). miR-155 expression also correlated significantly with poor outcomes for chordoma patients (hazard ratio, 5.32; p = 0.045).
Furthermore, using functional assays and The Cancer Genome Atlas (TCGA) Lung Adenocarcinoma (LUAD) dataset, we found that rs767649 variant allele could increase the transcriptional activity of miR-155, which in turn facilitated tumor growth and metastasis by inhibiting HBP1, TJP1, SMAD5 and PRKAR1A expression.
Before PRFA, tumor suppressor let-7a and miR-34a were downregulated whereas oncomiR miR-21 was upregulated in primary tumors, and let-7a and miR-126 levels were downregulated whereas oncomiRs miR-21, miR-155 and miR-17-5p/miR-20b levels were upregulated in secondary tumors.