Long non-coding RNAs (lncRNAs) are emerging as important modulators of cancer progression, among which prostate cancer-associated transcript 1 (PCAT1) has been shown to be an oncogene in several tumors. However, the clinical significance and biological function of PCAT1 in endometrial carcinoma (EC) remain unclear. In this study, we used 89 EC tissues and HEC-1B, Ishikawa, RL95-2 and AN3CA EC cell lines. We found elevated expression levels of PCAT1 in EC tissues and cell lines using reverse transcription qPCR (RT-qPCR). The prognostic value of PCAT1 was determined using Kaplan–Meier survival and Cox regression analysis. The results showed that higher PCAT1 expression was positively correlated with FIGO stage, myometrial invasion, lymph node metastasis, and a shorter overall survival. A series of functional assays showed that the knockdown of PCAT1 by small interfering RNA (siRNA) targeting PCAT1 (siPCAT1) suppressed cell proliferation, migration and invasion, but promoted apoptosis. Western blot analysis further showed that B-cell lymphoma 2 (Bcl-2), vimentin and N-cadherin were downregulated, but E-cadherin and Bcl-2-associated death promoter (Bad) were upregulated in PCAT1-silenced EC cells. Taken together, our results underscore the oncogenic role of PCAT1 in EC and show that PCAT1 may be a potential therapeutic target in EC treatment.

Pre-B-cell leukemia homeobox 3 (PBX3) is upregulated in various malignancies; however, the role of PBX3 in cervical cancer (CC) is unknown. The purpose of this study was to explore the expression characteristics, clinicopathological significance, and molecular biological function of PBX3 in CC. The expression levels of PBX3 were analyzed in CC cell lines and tumor specimens by real-time polymerase chain reaction (RT-PCR), Western blotting, and immunohistochemical staining. The clinicopathological characteristics associated with PBX3 expression were evaluated. An RNA interference approach was employed to suppress PBX3 expression in CC in vitro and in vivo, determine its role in cell proliferation and analyze its molecular function. We found that PBX3 expression was significantly upregulated in CC cell lines and clinical specimens compared with normal cells and adjacent nontumorous cervical tissues. PBX3 was an independent predictive factor of poor prognosis, and its expression was correlated with tumor diameter, pathological grading, lymph node metastasis, invasion depth, vascular invasion, and clinical stage of CC. Multivariate analysis suggested that PBX3 expression may represent an independent prognostic indicator of the survival of CC patients. CC patients with high PBX3 expression exhibited reduced overall survival compared with those with low PBX3 expression. Additionally, stable downregulation of PBX3 expression in CC cell lines suppressed cell proliferation and decreased p-AKT protein expression levels in vitro. Similarly, in vivo assays demonstrated that PBX3 downregulation in CC cells markedly inhibited tumor size and weight. Overall, we demonstrated that PBX3 can promote CC cell proliferation via the AKT signaling pathway and that it may serve as a prognostic marker. Our data indicate that inactivation of PBX3 may be an effective clinical treatment for CC.

Aim: Research on novel mutant genes may develop the treatment of cervical cancer (CC). The role of miRNA-526b in epithelial–mesenchymal transition (EMT) of CC was investigated. Methods: The role and the molecular mechanism of miRNA-526b in CC and its effect on EMT were analyzed in clinical specimens and oncology experiments. Results: miRNA-526b was proved to be decreased in CC and associated with malignant clinicopathological characters. The character of miRNA-526b in EMT was also inspected in CC cells and tumor models. miRNA-526b was found to be able to inhibit the EMT property of CC cells by directly targeting PBX3. Conclusion: miRNA-526b restoration may be deliberated as a new treatment strategy of CC.

This study aimed to determine the expression of microRNA (miRNA or miR)-378 in peripheral blood from patients with pregnancy-induced hypertension (PIH), and to try to understand its effect on vascular endothelial injuries induced by PIH. The study included 33 PIH patients. Quantitative real-time polymerase chain reaction was used to determine the expression of miR-378 in peripheral blood and NK cells. NK cells were transfected with miR-378 mimics and its negative control. Bioinformatics was used to predict the potential target gene of miR-378. Flow cytometry and Western blotting were performed to identify changes in the expression of CD226 protein. By co-culturing HUVECs with NK cells, the effects of miR-378 and CD226 on the proliferation, migration and apoptosis of HUVECs were evaluated. The results showed that the expression of miR-378 in peripheral blood was down-regulated with the progression of PIH. The expression of miR-378 was reduced in innate immune NK cells from peripheral blood of PIH patients. miR-378 negatively regulated the expression of CD226 in NK cells, and CD226 is a target gene of miR-378. miR-378 inhibited the expression and secretion of soluble CD226 by NK cells. miR-378 regulated the proliferation, migration and apoptosis of HUVECs by affecting the levels of soluble CD226 expressed by NK cells. The present study demonstrates that miR-378 is down-regulated in peripheral blood and NK cells from patients with PIH, and negatively correlated with the development of PIH. miR-378 protects HUVECs from injuries by soluble CD226 through down-regulating the expression of soluble CD226 in NK cells.