Novel tumor-targeting titanium dioxide (TiO2) nanoparticles modified with hyaluronic acid (HA) were developed to explore the feasibility of exploiting the pH-responsive drug release property ofTiO2and the tumor-targeting ability of HA to construct a tumor-targeting cisplatin (CDDP) delivery system (HA-TiO2) for potential neoadjuvant chemotherapy of ovarian cancer. The experimental results indicated that CDDP release from the HA-TiO2nanoparticles was significantly accelerated by decreasing pH from 7.4 to 5.0, which is of particular benefit to cancer therapy. CDDP-loaded HA-TiO2nanoparticles increased the accumulation of CDDP in A2780 ovarian cancer cells via HA-mediated endocytosis and exhibited superior anticancer activityin vitro.In vivoreal-time imaging assay revealed that HA-TiO2nanoparticles possessed preferable tumor-targeting ability which might potentially minimize the toxic side effects of CDDP in clinical application.

Uterine leiomyoma (UL) is the most common type of benign tumor in the women's reproductive system. A number of genes has been found to play an important role in the initiation and progression of UL, including miRNAs. In this study, our results exhibited that miR‐93, a member of mir‐106b‐25 cluster, significantly reduced the cell viability, promoted cell cycle arrest, caused apoptosis, and inhibited migration in UL cells (p < .01). Moreover, our results have provided experimental evidence that miR‐93 regulated the biological functions of UL cells by targeting CCND1.

Insufficient invasion of trophoblasts is known to be associated with preeclampsia (PE) development. Recently, microRNAs (miRNAs) have been reported to serve important roles in the pathogenesis of PE. However, little is known regarding the regulation of trophoblastic invasion by miRNAs. The aim of the present study was to explore the role of miRNAs in trophoblastic invasion and the underlying molecular mechanism. Using a miRNA microarray, miRNAs putatively involved in the pathophysiology of PE were examined between normal and preeclamptic placentas. Validation analysis of miR-142-3p level in placenta specimens was performed using reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Then, the regulation of miR-142-3p on trophoblast cells migration and invasion was evaluated using wound healing and transwell migration assays. Furthermore, the target gene of miR-142-3p and the downstream signaling pathway were also investigated. Microarray analysis and RT-qPCR revealed that miR-142-3p was significantly upregulated in placenta specimens from patients with PE. Its overexpression inhibited trophoblast cell invasion and migration, whereas its knockdown enhanced trophoblast cell invasion and migration. In addition, overexpression of miR-142-3p inhibited the mRNA expression and the activities of matrix metalloproteinase-2 (MMP2) and MMP9, which are closely associated with cell invasion and migration, while inhibition of miR-142-3p had the opposite result. Subsequent analyses demonstrated that transforming growth factor-β1 (TGF-β1) was a direct and functional target of miR-142-3p. Notably, the knockdown of TGF-β1 effectively reversed the enhancement of miR-142-3p inhibitor on trophoblast cell invasion and migration. Finally, the present study confirmed that miR-142-3p inhibitor enhanced cell invasion and migration by reactivating the TGF-β1/Smad3 signaling pathway. Taken together, the results of the present study suggest that miR-142-3p may serve an important role in human placental development by suppressing trophoblast cell invasion and migration through disruption of the TGF-β1/smad3 signaling pathway, suggesting that knockdown of miR-142-3p may provide a novel therapy for PE.