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The pentraxin is a superfamily of proteins with the same domain known as the pentraxin domain at C-terminal. This family has two subgroups, namely; short pentraxins (C-reactive protein and serum amyloid P component) and long pentraxins (neuronal pentraxin 1, neuronal pentraxin 2, neuronal pentraxin receptor, pentraxin 3 and pentraxin 4). Each group shares a similar structure with the pentameric complexes arranged in a discoid shape. Previous studies revealed the functions of different pentraxin family members. Most of them are associated with human innate immunity. Inflammation has commonly been associated with tumor progression, implying that the pentraxin family might also participate in tumor progression. Therefore, we reviewed the basic characteristics and functions of the pentraxin family and their role in tumor progression.

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In the present study, 203 patients that had previously undergone microsurgery for craniopharyngiomas (CPs) between 1992 and 2012 were analyzed retrospectively on a long-term follow-up basis to investigate the differences in the recurrence rate and endocrine function between patients with preserved and resected pituitary stalks. To summarize the possible outcomes of microsurgery, the 203 patients were divided into 2 groups: Group A that had preserved pituitary stalks and Group B that had undergone resections of the pituitary stalk. Tumor origins and the involvement of the pituitary stalk during surgery were observed. From 2010 onwards, an ultra-electron microscope was used postoperatively to detect whether pituitary stalk specimens were infiltrated or invaded with tumor cells. Long-term follow-up observations of the patients included tumor recurrence, postoperative endocrine dysfunction and visual acuity and field. Among the 203 patients, 175 patients received gross-total resection (GTR) (175/203, 86.2%), 28 patients underwent subtotal resection (28/203, 13.8%) and 34 patients had surgery that preserved the pituitary stalk (34/203, 16.7%). There was no significant difference in the recurrence rate between Group A (4/34, 11.8%) and the patients in Group B (10/123, 8.1%) who underwent GTR and also received follow-ups. Of the 157 patients who were followed up, 91 individuals underwent endocrine evaluation and the outcome was divided into normal, satisfactory and poor grades. The results for Group A were 5, 18 and 0, respectively, while the results for Group B were 1, 60 and 7, respectively, which showed a statistically significant difference between the groups. Pituitary stalk specimens of 15 patients were studied postoperatively using an ultra-electron microscope and all samples showed tumor cells had invaded the pituitary stalk (15/15, 100%). Total resections of CPs with the pituitary stalk were recommended if the pituitary stalk was intraoperatively invaded. In cases where the pituitary stalk was not involved, microsurgical excisions preserving the pituitary stalk were preferred, as there was no significant increase in the recurrence rate and the patients experienced less endocrine dysfunction.

A number of microRNAs have been identified to be important regulators of tumorigenesis. Previous research has shown that miR-124 is abundantly expressed in normal brain tissue; however, only a few reports have focused on the biological impact of miR-124 on glioma cells, and the underlying mechanisms need to be elucidated. Therefore, we investigated the effect of miR-124a on glioma cell proliferation and invasion; furthermore, the underlying molecular mechanism was examined. The present study demonstrated that miR-124a expression was downregulated in human glioma tissues, and its expression level was negatively correlated with the pathological grade of the glioma. Restoration of miR-124a inhibited glioma cell proliferation and invasion in vitro. Furthermore, we found that miR-124a directly targeted and suppressed IQ motif containing GTPase activating protein 1 (IQGAP1), a well-known regulator of actin dynamics and cell motility. RNA interference assay showed that IQGAP1 knockdown led to downregulation of β-catenin and downstream cyclin D1. Taken together, our study revealed that miR-124a could inhibit glioma cell proliferation and invasion by blocking the expression of the IQGAP1 gene and downstream β-catenin and cyclin D1. This research may provide a useful molecular therapy for gliomas.

AbstractBackgroundFibrosis in the ventricular system is closely associated with post-hemorrhagic hydrocephalus (PHH). It is characterized by an expansion of the cerebral ventricles due to CSF accumulation following intraventricular hemorrhage (IVH). The activation of transforming growth factor-β1 (TGF-β1) may be involved in thrombin-induced arachnoid fibrosis.MethodsA rat model of PHH was established by injection of autologous non-anticoagulated blood from the right femoral artery into the lateral ventricles. Differential expression of miR-30a was detected in rat arachnoid cells by RNA sequencing. AP-1, c-Fos, and TRAF3IP2 were knocked down in primary arachnoid cells, and the degree of arachnoid fibrosis was assessed.ResultsDecreased expression of miR-30a and increased expression of TRAF3IP2, TGF-β1, and α-SMA were detected in the arachnoid cells of PHH rat. Besides, overexpression of miR-30a targets TRAF3IP2 mRNA 3′UTR and inhibits the expression of TRAF3IP2, TGF-β1, and α-SMA in the primary arachnoid cells. Furthermore, TRAF3IP2 activates AP-1 to promote arachnoid fibrosis. The content of type I collagen in the primary arachnoid cells was reduced after the silencing of AP-1 and TRAF3IP2.ConclusionsThis study identified a miR-30a-regulated mechanism of arachnoid fibrosis, suggesting a previously unrecognized contribution of miR-30a to the pathogenesis of fibrosis in the ventricular system. These results might provide a new target for the clinical diagnosis and treatment of PHH.