MiR‐30a‐5p inhibits proliferation and metastasis of hydatidiform mole by regulating B3GNT5 through ERK/AKT pathways

Abstract

Hydatidiform moles are gestational trophoblastic disease. They are abnormal proliferations of trophoblast cells that have the potential to become cancerous. miR‐miR30a‐5p is a tumour suppressor that participates in the development of numerous diseases. However, the role of miR‐30a in hydatidiform moles and the mechanisms underlying its effects are presently unclear. This study explored the levels of miR‐30a and B3GNT5 expression in human hydatidiform mole tissue. The results showed that miR‐30a and B3GNT5 were differentially expressed in normal placenta and hydatidiform mole, and miR‐30a decreased cell proliferation, invasion and migration in trophoblast cell lines. Upon further examination, it was confirmed that miR‐30a directly targeted the 3’untranslated region of B3GNT5 using a dual‐luciferase assay. The results of the present study also revealed that miR‐30a reduced the proliferation, invasion and migration ability in JAR and BeWo cells by regulating B3GNT5, which may inactivate the ERK and AKT signalling pathways. This study demonstrated that miR‐30a was a novel target B3GNT5 that serves an important role in the development of hydatidiform moles, suggesting that miR‐30a may serve as a novel potential biomarker or useful diagnostic and therapeutic tool for hydatidiform moles in clinical settings.

STOX2 Is the Target of Mir-30a to Increase Cell Proliferation and Metastasis in Hydatidiform Mole Through ERK, AKT and P38 Signaling Pathways

“…In previous studies, we demonstrated that the expression level of miR-30a was lower in hydatidiform moles which can be seen in our earlier article [49] . However, the regulatory mechanism of miR-30a in hydatidiform mole is still unclear.…”

miR-30a targets STOX2 to increase cell proliferation and metastasis in hydatidiform moles via ERK, AKT, and P38 signaling pathways

“…In our previous study, we demonstrated that the expression level of miR-30a was lower in hydatidiform moles [ 30 ]. However, the regulatory mechanism of miR-30a in hydatidiform moles is still unclear.…”

“…Among them, miR-30a was the miRNA with the largest differential multiple. Therefore, we further investigated miR-30a and found that it had low expression in hydatidiform mole tissue [ 30 ]. In addition, we found that miR-30a can affect the occurrence of hydatidiform moles by regulating UDP-GlcNAc:betaGal beta-1,3-N-acetylglucosaminyltransferase 5 (B3GNT5).…”

Circular RNA PUM1 (CircPUM1) attenuates trophoblast cell dysfunction and inflammation in recurrent spontaneous abortion via the MicroRNA-30a-5p (miR-30a-5p)/JUNB axis

“…Among the 11 miRNAs predicted (miR-2682-5p, miR-34b-5p, miR-449 c-5p, miR-545-5p, miR-30b-5p, miR-30a-5p, miR-30e-5p, miR-30 c-5p, miR-30d-5p, miR-770-5p, and miR-4712-5p), miR-30a-5p expression was remarkably higher in HTR-8/SVneo cells transfected with si-circPUM1 ( Figure 2a ). It has been demonstrated by previous reports that miR-30a-5p represses cell viability, migration, and invasion, accelerates cell apoptosis, and exacerbates inflammatory response [ 25–27 ]. Therefore, miR-30a-5p was selected as the target miRNA for circPUM1 in this work.…”

“…Zhang et al disclosed that miR-30a-5p conferred inflammation in myocarditis-induced cardiac injury via regulating SOCS1 [ 42 ]. Moreover, Guo et al uncovered that miR-30a-5p impaired proliferation and metastasis of trophoblast cells through the ERK/AKT pathway via targeting B3GNT5 [ 25 ]. Herein, rescue assays also demonstrated that circPUM1 facilitated proliferation, migration, and invasion, but suppressed apoptosis and proinflammatory secretion in trophoblast cells as a sponge for miR-30a-5p.…”