The results indicated that miR‑30a‑3p suppressed metastasis and enhanced the radiosensitivity of EC cells via downregulation IGF‑1R, suggesting that miR‑30a‑3p may be a potential therapeutic target in the treatment of EC.
MTDH, SKP2, BCL9, and NOTCH1 genes were overexpressed in ovarian cancer cells, and they are direct target genes of miR-30a-5p. miR-30a-5p overexpression inhibited epithelial-mesenchymal transition (EMT) process, while upregulation of SKP2, BCL9, and NOTCH1 gene expression levels reduced the inhibition of EMT process by miR-30a-5p. miR-30a-5p was lowly expressed in ovarian cancer, and such a phenomenon is related to ovarian cancer metastasis. miR-30a-5p might inhibit the migration and invasion of ovarian cancer cells by downregulating the expression of SKP2, BCL9, and NOTCH1 genes.
Interestingly, overexpression of MEF2D partially reversed the miR-30a-reduced cell proliferation, migration, and invasion of osteosarcoma cell, indicating that miR-30a suppresses osteosarcoma cell proliferation and metastasis partially mediated by inhibition of MEF2D.
Collectively, this study indicated that miR‑30a functions as a tumor‑metastasis suppressor miRNA in TNBC by directly targeting ROR1 and that miR‑30a may serve as a novel therapeutic target for TNBC.
MiR-30a-5p attenuates the EMT and metastasis in GBC cells by targeting E2F7, suggesting miR-30a-5p is a tumour suppressor that may serve as a novel potential prognostic biomarker or molecular therapeutic target for GBC.
Norcantharidin modulates the miR-30a/Metadherin/AKT signaling axis to suppress proliferation and metastasis of stromal tumor cells in giant cell tumor of bone.
Moreover, miR-30a has demonstrated its role in biological processes, including inhibiting proliferation and metastasis in many tumors, autophagy in chronic myelogenous leukemia, and regulating TGF-b1-induced epithelial-mesenchymal transition.
Validation by RT-qPCR in a LAC cohort comprising 52 patients confirmed that decreased expression of miR-30a-3p and increased expression of miR-210-3p were significantly associated with the presence of distant metastases. miR-210-3p tumor cell specificity was evaluated by in situ hybridization and its biomarker potential was confirmed by ROC curve analysis (AUC = 0.839).
Overall, these findings demonstrated that miR-30a might play a certain role in the cell growth, apoptosis and metastasis of HCC cells, partially via regulating K-Ras/c-Raf/MEK/ERK signaling pathway, potentially, it is therefore a candidate targeting biomarker for HCC therapy.
MicroRNA-30a increases tight junction protein expression to suppress the epithelial-mesenchymal transition and metastasis by targeting Slug in breast cancer.
Importantly, overexpression of ITGB3 in colorectal cancer cells rescued these cells from miR-30a-5p-mediated suppression of metastasis and restored the epithelial-mesenchymal transition.
These results suggested the potential linkage between miR-30a and genes (AEG-1, Snail and Vimentin) in the epithelial-mesenchymal transition and metastasis of lung tumor cell.
Integrated analyses allow understanding the interplay between different levels of molecular alterations.We integrated miRNA and gene expression data from 458 ccRCC and 254 normal kidney specimens to construct a miRNA-target interaction network.We identified the downregulated miR-124-3p, -30a-5p and -200c-3p as the most influential miRNAs in RCC pathogenesis.miR-124-3p and miR-200c-3p expression showed association with patient survival, miR-30a-5p was downregulated in metastases compared to primary tumors.
We identified SNAI1 as a direct target of miR-30a and demonstrated miR-30a as a novel regulator of EMT by targeting SNAI1, indicating its potential therapeutic value for reducing invasion and metastasis of HCC.