[Retracted] MicroRNA­19b promotes the migration and invasion of ovarian cancer cells by inhibiting the PTEN/AKT signaling pathway.

[This retracts the article DOI: 10.3892/ol.2018.8695.].

CTRP family in diseases associated with inflammation and metabolism: molecular mechanisms and clinical implication.

C1q/tumor necrosis factor (TNF) related proteins (CTRPs) is a newly discovered adipokine family with conservative structure and ubiquitous distribution and is secreted by adipose tissues. Recently, CTRPs have attracted increasing attention due to the its wide-ranging effects upon inflammation and metabolism. To-date, 15 members of CTRPs (CTRP1-15) with the characteristic C1q domain have been characterized. Earlier in-depth phenotypic analyses of mouse models of CTRPs deficiency have also unveiled ample function of CTRPs in inflammation and metabolism. This review focuses on the rise of CTRPs, with a special emphasis on the latest discoveries with regards to the effects of the CTRP family on inflammation and metabolism as well as related diseases. We first introduced the structure of characteristic domain and polymerization of CTRPs to reveal its pleiotropic biological functions. Next, intimate association of CTRP family with inflammation and metabolism, as well as the involvement of CTRPs as nodes in complex molecular networks, were elaborated. With expanding membership of CTRP family, the information presented here provides new perspectives for therapeutic strategies to improve inflammatory and metabolic abnormalities.

SP1-induced up-regulation of lncRNA LUCAT1 promotes proliferation, migration and invasion of cervical cancer by sponging miR-181a.

Long noncoding RNA lung cancer associated transcript 1 (LUCAT1) has been shown to be a lncRNA that facilitates the development and progression of several tumours. However, the evidence of LUCAT1 modulating the growth and metastasis of cervical cancer (CC) were still lacking. The present study aimed to explore the expression pattern, biological function and potential mechanism of LUCAT1 in CC. In this study, we, first, confirmed that LUCAT1 acted as an up-regulated lncRNA by analyzing the data from GCTA dataset and RT-PCR in both CC tissues and cell lines. We also showed that TINCR overexpression is induced by nuclear transcription factor SP1. Then, clinical assays showed that LUCAT1 was associated with advanced clinical progression and poor prognosis of CC patients. Importantly, multivariate Cox model confirmed that LUCAT1 expression was an independent prognostic factor for both 5-year overall survival in CC. Then, lost-function assays revealed that knockdown of LUCAT1 significantly suppressed CC cells proliferation, colony formation, migration, invasion and EMT by a series of cells experiments. Mechanistically, Bioinformatic tools predicted that miR-181a may target LUCAT1, which was confirmed using luciferase reporter assay and RNA immunoprecipitation (RIP) assays. Overall, our findings showed that SP1-activated LUCAT1 exerts an oncogenic function in CC by binding to miR-181a, suggesting that miR-181a may be a ponderable and promising therapeutic target for CC.

MicroRNA-19b promotes the migration and invasion of ovarian cancer cells by inhibiting the PTEN/AKT signaling pathway.

Local and systemic metastasis is the main reason for the poor survival rate of patients with ovarian cancer (OC). MicroRNAs (miRNAs/miRs) are short non-coding RNAs that serve critical roles in the initiation and progression of OC. The present study demonstrated that expression of miR-19b was significantly increased in OC tissues and cell lines. Analysis of clinicopathological features revealed that the increased expression of miR-19b was associated with advanced International Federation of Gynecology and Obstetrics stage and lymphatic metastasis of OC patients. Loss-of-function experiments demonstrated that the silencing of miR-19b reduced the migration and invasion of OVCAR-3 cells; contrarily, the overexpression of miR-19b facilitated the migration and invasion of CAOV-3 cells. Furthermore, miR-19b regulated the expression of phosphatase and tensin homolog (PTEN) and the activity of the PTEN/RAC serine/threonine-protein kinase pathway in vitro. Notably, the results of dual-luciferase reporter assays indicated that PTEN was a direct downstream target of miR-19b in OC. Taken together, the results of the current study demonstrated that miR-19b serves an oncogenic role in the progression of OC, and could potentially act as a biomarker and therapeutic target for OC patients.

Study on the mesothelin-specific cytotoxicity against epithelial ovarian cancer with full-length mesothelin cDNA-transduced dendritic cells.

Epithelial ovarian cancer (EOC) has the highest mortality rate among the various types of gynecological cancers. As the current therapeutic approaches are not enough, the development of more effective treatments to improve the survival of patients with EOC is urgently needed. Mesothelin (MSLN) is a cell surface glycoprotein, which is overexpressed in ovarian cancer tissues. As an immunotherapeutic approach, in this study, we investigated whether the genetically modified dendritic cells (DCs) expressing MSLN could induce cytotoxic T lymphocytes (CTLs) to produce MSLN-specific cytotoxic activity against EOCs. Here, we report that DCs transfected with full-length coding sequence of MSLN could induce MSLN-specific CTLs responses against ovarian cancer lines SKOV3 and OVCAR3 in vitro. Additionally, we identified that the death rates of ovarian cancer cells, killed by MSLN-specific CTLs, were significantly higher than the normal CTLs. Furthermore, IFN-γ production by stimulated MSLN-specific CTLs was significantly higher than that of unstimulated CTLs. This study showed that induced CTLs by DCs with full-length MSLN cDNA have effective immune response against the ovarian cancer cells, indicating that MSLN-transfected DCs vaccine has a promising prospect for the treatment of EOC.