Identification of Differentially Expressed microRNAs in Metastatic Ovarian Cancer

Abstract

Background: The molecular mechanisms of ovarian cancer (OC) remain unclear. We sought to comprehensively identify miRNAs that are aberrantly expressed in OC. Methods: Differentially expressed miRNAs were screened from six pairs of primary and metastatic OC tissues; their possible functions were then analyzed and target genes were predicted by bioinformatics. Then gene expression profiling results were established by reverse transcription quantitative polymerase chain reaction and western blot. Target binding between miR-7-5p and TGFβ2 was validated by dual-luciferase reporter assay. Results: Fifteen miRNAs and 10 target mRNAs were differentially expressed in primary and metastatic OC tissues. ITGB3, TGFβ2 and TNC correlated to miRNA function in metastatic OC. Compared with primary OC, RNA levels of hsa-miR-141-3p, hsa-miR-7-5p and hsa-miR-187-5p in metastatic OC tissues were potently decreased ( p < 0.05). However, a statistically prominent difference in hsa-miR-584-5p level between the two groups ( p > 0.05) was not observed. Comparing to primary OC, TGFβ2 and TNC were markedly increased ( p < 0.05). Luciferase activity was remarkably decreased after co-transfection of a wild-type TGFβ2 3’-UTR plasmid and miR-7-5p compared with a control plasmid, but no remarkable change after co-transfection of mutant TGFβ2 3’-UTR and miR-7-5p was demonstrated. Conclusions: Fifteen miRNAs and 10 mRNAs were differentially expressed in metastatic OC tissues compared with primary OC tissues, which suggested that they may participate in invasive and metastatic processes. Hsa-miR-141-3p, hsa-miR-187-5p and hsa-miR-7-5p expression was prominently lower in metastatic OC than in primary OC, while TGFβ2 and TNC expression was markedly higher in metastatic OC tissues. Hsa-miR-7-5p may bind to the TGFβ2 3’-UTR to inhibit its expression.

Chondrocyte suppression is mediated by miR‐129‐5p via GDF11/SMAD3 signaling in developmental dysplasia of the hip

“…As intrinsic regulators, miRNAs have been shown to play critical roles in chondrocyte proliferation, differentiation, and endochondral ossification 16‐19 . In addition, aberrant miRNA expression is involved in many bone‐related disorders, including osteoarthritis, osteoporosis, and bone tumors 20‐22 . To the best of our knowledge, the role of miRNAs in the endochondral ossification of the acetabular roof has not yet been analyzed in the DDH setting.…”

MicroRNA‐210‐3p Promotes Chondrogenic Differentiation and Inhibits Adipogenic Differentiation Correlated with HIF‐3α Signalling in Bone Marrow Mesenchymal Stem Cells

“…Our experiment investigated the ability of miR-210 stem cells to differentiate into chondrogenic and adipogenic lineages. Many studies have demonstrated that miR-210 promotes osteogenic differentiation of stem cells [22][23][24][25]. Notably, the results of Li et al [22] demonstrated that miR-210 promoted osteogenic differentiation of rat bone marrow stem cells.…”

A Signature of Circulating miRNAs Associated With Fibrous Dysplasia of Bone: the mirDys Study

“…miR‐324‐5p is increased in end‐stage osteoarthritis by regulating hedgehog signaling and osteogenesis in human MSCs ( 53 ) and it is also downregulated in the bone marrow of osteoporotic patients. ( 54 ) By searching in the miRWalk database, we have found that miR‐324‐5p targets three genes (FOXO1/FOXO3, FOSB, and RUNX2) that promote osteoblastogenesis and consequently would interfere negatively with osteoblast differentiation and bone mineralization. Karvande and colleagues ( 55 ) have shown that the bone formation induced by PTH therapy was related to the increase in miR‐451a serum levels.…”