Prognostic marker VPS72 could promote the malignant progression of prostate cancer.

BACKGROUND: This paper attempted to clarify the role and mechanism of vacuolar protein sorting-associated protein 72 homolog (VPS72) in the progression of prostate cancer (PCa). METHODS: Clinical information and gene expression profiles of patients with prostate cancer were obtained from The Cancer Genome Atlas (TCGA). VPS72 expression in PCa and the potential mechanism by which VPS72 affects PCa progression was investigated. Next, we performed COX regression analysis to identify the independent prognostic factors of PCa, and constructed a nomogram. The sensitivity of chemotherapeutic medications was anticipated using "pRRophetic". Subsequently, in vitro assays to validate the effect of VPS72 on PCa cell proliferation, migration and susceptibility to anti-androgen therapy. RESULTS: The expression of VPS72 was considerably higher in PCa tissues compared to normal tissues. Significant correlations were found between high VPS72 expression and a poor prognosis and adverse clinicopathological factors. The nomogram model constructed based on VPS72 expression has good predictive performance. According to GSEA, VPS72-related genes were enriched in the NF-kB pathways, cytokine-cytokine receptor interaction and chemokine signaling pathway in PCa. Although PCa with low VPS72 expression was more adaptable to chemotherapeutic medications, our in vitro experiment showed that VPS72 knockdown significantly decreased the PCa cell migration, proliferation, and resistance to anti-androgen therapy. CONCLUSIONS: In summary our findings suggests that VPS72 could play a crucial role in the malignant progression of PCa, and its expression level can be employed as a possible biomarker of PCa prognosis.

Which Surface Is More Scaling Resistant? A Closer Look at Nucleation Theories for Heterogeneous Gypsum Nucleation in Aqueous Solutions.

Developing engineered surfaces with scaling resistance is an effective means to inhibit surface-mediated mineral scaling in various industries including desalination. However, contrasting results have been reported on the relationship between scaling potential and surface hydrophilicity. In this study, we combine a theoretical analysis with experimental investigation to clarify the effect of surface wetting property on heterogeneous gypsum (CaSO4·2H2O) formation on surfaces immersed in aqueous solutions. Theoretical prediction derived from classical nucleation theory (CNT) indicates that an increase of surface hydrophobicity reduces scaling potential, which contrasts our experimental results that more hydrophilic surfaces are less prone to gypsum scaling. We further consider the possibility of nonclassical pathway of gypsum nucleation, which proceeds by the aggregation of precursor clusters of CaSO4. Accordingly, we investigate the affinity of CaSO4 to substrate surfaces of varied wetting properties via calculating the total free energy of interaction, with the results perfectly predicting experimental observations of surface scaling propensity. This indicates that the interactions between precursor clusters of CaSO4 and substrate surfaces might play an important role in regulating heterogeneous gypsum formation. Our findings provide evidence that CNT might not be applicable to describing gypsum scaling in aqueous solutions. The fundamental insights we reveal on gypsum scaling mechanisms have the potential to guide rational design of scaling-resistant engineered surfaces.

The Contrary Effects of Sirt1 on MCF7 Cells Depend on CD36 Expression Level.

BACKGROUND: Breast cancer is one of the most aggressive and pervasive cancers identified in females. Sirt1 and CD36 both exert an essential role toward the oncogenic signaling in breast cancer cells. As reported, the adrenergic signaling could promote the malignancy of breast cancer. This study focuses specifically on the role of Sirt1/CD36 in the proliferation of MCF-7 breast cancer cells and also investigates their response to the α2-adrenergic agonist dexmedetomidine (Dex). MATERIALS AND METHODS: Expression of Sirt1 and CD36 was measured in breast cancer tissue by immunohistochemistry. We cultured MCF7 cells and treated cells with resveratrol (RSV) or Dex. Western blot analysis was performed to quantify the protein expression levels. The methyl thiazolyl tetrazolium (MTT) assay was applied to detect cell proliferation. RESULTS: Compared with normal adjacent tissues, Sirt1 increased and CD36 decreased in cancer tissues. RSV, a Sirt1 activator, increased the proliferation of MCF-7 cells at low concentration but exerted cytotoxicity effect at higher concentration. Sirt1 activation increased the expression of CD36 at higher concentration. Dex treatment gradually increased the proliferation of MCF7 cells in a dose-dependent manner and downregulated the expression of Sirt1/CD36. Interestingly, overexpression of Sirt1 via RSV pretreatment could suppress Dex-stimulated proliferation of breast cancer, accompanied with CD36 upregulation. CONCLUSIONS: though expression of Sirt1 increased in breast cancer progression, overexpression of Sirt1 could inhibit MCF7 proliferation, which may be associated with CD36 upregulation. In addition, the promotion effect of Dex on MCF7 cells, which may be associated with the Sirt1/CD36 inhibition, could be weakened by Sirt1 activation via RSV.

Knockdown of NUPR1 inhibits the proliferation of glioblastoma cells via ERK1/2, p38 MAPK and caspase-3.

Nuclear protein-1 (NUPR1), located on chromosome 16p11.2, is a stress response factor that plays an important role in the growth and migration of human malignant tumor cells. However, the role of NUPR1 in glioblastoma remains poorly understood. The expression level of NUPR1 was detected by quantitative real-time PCR and immunohistochemistry (IHC). Wound healing, MTT, cell counting and BrdU assays were used to analyze the migration and proliferation of glioblastoma cells after down-regulating NUPR1 expression using a lentiviral vector. FACS analysis and a signaling antibody array kit were used to detect the mechanism by which NUPR1 modulates cell cycle and apoptosis activities in glioblastoma cells. We confirmed that NUPR1 was up-regulated in glioblastoma tissues compared to NB tissues. Down-regulation of NUPR1 suppressed cell migration and proliferation, arrested the cell cycle in the G0/G1 phase and promoted apoptosis in U251 and U87 cells in vitro. Furthermore, the expression levels of phosphorylated ERK1/2, p38 MAPK and cleaved caspase-3 were decreased upon silencing NUPR1 expression in U251 and U87 cells. In summary, NUPR1 plays an important role in the growth and migration of human glioblastoma cells. Knockdown of NUPR1 suppressed glioblastoma cell growth by arresting the cell cycle and inducing cell apoptosis via decreases in the expression of ERK1/2, p38 MAPK and caspase-3.

Down-regulation of ribosomal protein S15A inhibits proliferation of human glioblastoma cells in vivo and in vitro via AKT pathway.

Ribosomal protein s15a (RPS15A), a highly conserved cytoplasmic protein, promotes mRNA/ribosome interaction in translation. Recent evidence showed that RPS15A is essential for tumor growth. RPS15A expression level was measured in glioblastoma tissue samples and normal brain (NB) tissue samples. RPS15A RNAi stable cell line U87 and U251 was generated by the pLVTHM-GFP lentiviral RNAi expression system. The knockdown efficiency was confirmed by quantitative real-time PCR and western blot. Molecular mechanisms and the effect of RPS15A on cell growth and migration were investigated by using western blot, MTT assay, wound healing assay, transwell migration assay, and tumorigenesis in nude mice. Here, we report that RPS15A is overexpressed in human glioblastoma tumor tissues. RPS15A knockdown inhibits proliferation and migration of glioblastoma cells in vitro. Knocking down RPS15A leads to the level of p-Akt decrease and cell cycle arrested in G0/G1 phase in U87 and U251 cells. Furthermore, the growth of glioblastoma cell-transplanted tumors in nude mice is inhibited by transduction with Lv-shRPS15A. Our findings indicate that RPS15A promotes cell proliferation and migration in glioblastoma for the first time. RPS15A might play a distinct role in glioblastoma and serve as a potential target for therapy.

DNA damage-induced NF-κB activation in human glioblastoma cells promotes miR-181b expression and cell proliferation.

BACKGROUND: Glioblastoma (GBM) is the most common and most aggressive form of brain cancer. After surgery, radiotherapy is the mainstay of treatment for GBM patients. Unfortunately, the vast majority of GBM patients fail responding to radiotherapy because GBM cells remain highly resistant to radiation. Radiotherapy-induced DNA damage response may correlate with therapeutic resistance. METHODS: Ionizing radiation (IR) was used to induce DNA damage. Cell proliferation and migration were detected by wound-healing, MTT and apoptosis assays. Dual-luciferase assays and Western blot analysis were performed to evaluate NF-κB activation and validate microRNA targets. Real-time PCR was used to study mRNA and microRNA levels. RESULTS: IR-induced DNA damage activated NF-κB in GBM cells which promoted expression of IL-6, IL-8 and Bcl-xL, thereby contributing to cell survival and invasion. Knockdown SENP2 expression enhanced NF-κB essential modulator (NEMO) SUMOylation and NF-κB activity following IR exposure. miR-181b targets SENP2 and positively regulated NF-κB activity. CONCLUSION: NF-κB activation by DNA damage in GBM cells confers resistance to radiation-induced death.

Antiscalants for mitigating silica scaling in membrane desalination: Effects of molecular structure and membrane process.

Silica scaling is a major type of mineral scaling that significantly constrains the performance and efficiency of membrane desalination. While antiscalants have been commonly used to control mineral scaling formed via crystallization, there is a lack of antiscalants for silica scaling due to its unique formation mechanism of polymerization. In this study, we performed a systematic study that investigated and compared antiscalants with different functional groups and molecular weights for mitigating silica scaling in membrane distillation (MD) and reverse osmosis (RO). The efficiencies of these antiscalants were tested in both static experiments (for hindering silicic acid polymerization) as well as crossflow, dynamic MD and RO experiments (for reducing water flux decline). Our results show that antiscalants enriched with strong H-accepters and H-donors were both able to hinder silicic acid polymerization efficiently in static experiments, with their antiscaling performance being a function of both molecular functionality and weight. Although poly(ethylene glycol) (PEG) with abundant H-accepters exhibited high antiscaling efficiencies during static experiments, it displayed limited performance of mitigating silica scaling during MD and RO. Poly (ethylene glycol) diamine (PEGD), which has a PEG backbone but is terminated by two amino groups, was efficient to both hinder silicic acid polymerization and reduce water flux decline in MD and RO. Antiscalants enriched with H-donors, such as poly(ethylenimine) (PEI) and poly(amidoamine) (PAMAM), were effective of extending the water recovery of MD but conversely facilitated water flux decline of RO in the presence of supersaturated silica. Further analyses of silica scales formed on the membrane surfaces confirmed that the antiscalants interacted with silica via hydrogen bonding and showed that the presence of antiscalants governed the silica morphology. Our work indicates that discrepancy in antiscalant efficiency exists between static experiments and dynamic membrane filtration as well as between different membrane processes associated with silica scaling, providing valuable insights on the design principle and mechanisms of antiscalants tailored to silica scaling.

Β-elemene inhibits Hsp90/Raf-1 molecular complex inducing apoptosis of glioblastoma cells.

ß-Elemene, an active component of herb medicine Curcuma wenyujin, has been shown to antagonize glioblastoma cells by inducing apoptosis. However, how ß-elemene induces apoptosis of these cells remains unclear. In this study, we report that ß-elemene disrupted the formation of the Hsp90/Raf-1 complex, a key step in maintaining the conformation stability of Raf-1, and caused deactivation of Raf-1 and inhibition of the ERK pathway, thereby leading to apoptosis of glioblastoma cells. Specifically, treatment of glioblastoma cell lines with ß-elemene attenuated phosphorylation of multiple members of the kinase families in the Ras/Raf/MEK/ERK cascade, including Raf-1 and ERK as well as downstream signaling targets such as Bcl-2. These results suggest that the Hsp90/Raf-1 complex could be a promising molecular target for new drug development for the treatment of glioblastoma.

A pan-cancer analysis of ring finger protein 135 and its relationship to triple-negative breast cancer proliferation and metastasis.

Ring finger protein 135 (RNF135) is an E3 ubiquitin ligase with RING finger domains that plays a crucial role in the development of several forms of cancer. Neither the expression profile of RNF135 nor its importance in the diagnosis of pan-cancer have been elucidated as of yet. With the aid of The Cancer Genome Atlas and Gene Expression Omnibus, we have fully mapped the expression profiles, prognostic relevance, genetic modification, immune cell infiltration, and tumor heterogeneity of RNF135 in 33 malignant tumors. RNF135 was expressed inconsistently in various cancers, and variations in RNF135 expression predicted survival outcomes for cancer patients. There was a strong correlation between the levels of the RNF135 genetic mutation and some tumor progression. In addition, a strong correlation was seen between RNF135 expression and immune cell infiltration, tumor mutation burden, microsatellite instability, and immunoregulators. In contrast, the correlation between RNF135 expression and triple-negative breast cancer was investigated in this study. RNF135 may boost the proliferation, migration, and invasion of TNBC cells, according to cell experiments. RNF135 might be utilized as a biomarker to anticipate how a tumor will behave and may have a significant role in how TNBC cells grow and migrate, according to the findings of this study.

Clinical characteristics and treatment outcome of children with intraocular retinoblastoma: a report from a Chinese cooperative group.

BACKGROUND: To present the characteristics and treatment outcome of patients with intraocular retinoblastoma in a Chinese cooperative group. PROCEDURE: Between January 2005 and March 2009, 159 eyes of 133 patients with retinoblastoma were included in this retrospective study. The International Classification of Retinoblastoma (ICRB) staging system was noted for each patient. Cases with visible extraocular extension at diagnosis were excluded. The patient data were reviewed for demographic information, clinical findings, and managements. RESULTS: Of 133 cases, there were 83 (62%) male and 50 (38%) female, ranging in age from 2 months to 134 months (median, 23 months; mean, 26 months). There were 26 bilateral cases (20%). One hundred and twenty-four cases (93%) were deemed sporadic and nine cases (7%) were deemed familial. Leukocoria was the most common presenting symptom. One hundred and twenty-three eyes (77%) of 123 patients (92%) had no visual potential. Only 36 eyes (23%) of 30 patients (23%) utilized vision-preserving treatments. The ocular salvage rate was 83% (30/36) for this group. The cumulative probability of survival was 98% (Kaplan-Meier method) at 60 months follow up. CONCLUSIONS: The overall survival rate of this study is in agreement with data from developed countries. In appropriate patients, systemic chemotherapy, and focal ophthalmic therapy are effective and carry little morbidity. Compared with more medically developed countries, there are still many challenges in the management of retinoblastoma in China. Early detection and doctor education should be an important future goal. Pediatr Blood Cancer 2011; 57: 1113-1116. © 2011 Wiley Periodicals, Inc.

[Clinicopathologic features of retinoblastoma and expression of VEGF and Ki-67 after comprehensive treatment].

OBJECTIVE: To investigate the clinic pathologic features of retinoblastoma (RB) after comprehensive treatment, and study the expression of vascular endothelial growth factor (VEGF) in retinoblastoma treated with chemotherapy prior to enucleation. METHODS: Retrospective analysis was performed on retinoblastoma specimens obtained consecutively between 2006 and 2008 by enucleation, and patients' clinical information and clinic pathologic features were also collected. Immunohistochemical staining and real-time PCR were performed for the expression of VEGF. Immunohistochemical staining was also performed for Ki-67. RESULT: Among the 9 chemotherapy-treated cases, six belonged to group D and three to group E of IIRC. The reasons for enucleation included extensive vitreous seeds, RB recurrence, extensive subretinal fluid/seeds, vitreous hemorrhage and total tractional detachment of the retina. During the comprehensive treatment, the main tumors regressed in all eyes. The main tumors showed a mean decrease of 43.7% in the largest basal diameter and a mean decrease of 57.9% in thickness. The average interval between the end of chemotherapy and enucleation was 5.7 months. The reason for enucleation was the recurrence of main tumor, recurrence of new tumors, recurrent vitreous seed or subretinal seed. Three eyes showed a type 1 regression pattern, one eye showed a type 2 pattern, and the other five eyes showed type 3 clinical regression patterns. The expression of VEGF was lower in eyes that underwent planned enucleation than eyes that suffered from RB recurrence. CONCLUSIONS: The main reason for enucleation was extensive subretinal fluid/seeds after the comprehensive treatment. The type 3 clinical regression patterns were most common. In retinoblastoma, higher expression of VEGF may play an important role in the recurrence of retinoblastoma after comprehensive treatment.

A-kinase interacting protein 1 is sufficiently expressed and positively associates with WHO grade, meanwhile predicts unfavorable overall survival independently in glioma patients.

ABSTRACT: The present study aimed to investigate the association of A-kinase interacting protein 1 (AKIP1) with clinical characteristics, and further explore the prognostic value of AKIP1 in glioma patients.Totally 168 glioma patients who underwent tumor resection were analyzed, and their tumor tissue specimens were acquired for the detection of AKIP1 expression by immunohistochemistry (IHC), which was scored by a semi-quantitative method considering staining intensity and staining density.According to AKIP1 expression in tumor tissues of glioma patients, there were 65 (38.7%) patients with AKIP1 low expression (IHC score 0-3), 48 (28.6%) patients with AKIP1 high + expression (IHC score 4-6), 42 (25.0%) patients with AKIP1 high++ expression (IHC score 7-9) and 13 (7.7%) patients with AKIP1 high+++ expression (IHC score 10-12), respectively. AKIP1 expression was positively associated with World Health Organization grade. Overall survival (OS) was the lowest in the patients with AKIP1 high+++ expression, followed by those with AKIP1 high++ expression and those with AKIP1 high+ expression, and highest in those with AKIP1 low expression. Further subgroup analysis exhibited that AKIP1 expression was negatively associated with OS especially in high-grade glioma patients. In addition, AKIP1 expression was negatively associated with OS in all subgroups of patients with/without adjuvant radiotherapy, with/without adjuvant chemotherapy. Further multivariate Cox's regression exhibited that AKIP1 high expression was an independent predictive factor for worse OS.AKIP1 presents with the potential to be a novel biomarker for tumor management and prognosis surveillance in glioma patients.

Dioscin ameliorates diabetes cognitive dysfunction via adjusting P2X7R/NLRP3 signal.

Dioscin presents extents of pharmacological activities on several diseases, but its effect and mechanism on diabetes cognitive dysfunction (DCD) remains unclear. Herein, we conducted a series of pharmacological evaluation assays of purinergic receptor P2X7 (P2X7R) with dioscin. We uncovered that dioscin presented a clearly protective effect on diabetes cognitive dysfunction via a methylglyoxal-treated PC12 cell model and streptozocin (STZ)-induced rat models. Additionally, it found that P2X7R and NLRP3 inflammasome signals were activated in diabetes cognitive dysfunction via in vivo and in vitro detection. Moreover, it was demonstrated that P2X7R regulated NLRP3 inflammasome signals in methylglyoxal-treated PC12 cells. Meanwhile, it was showed that dioscin-induced anti-diabetes cognitive dysfunction effect was accompanied with an inhibition of P2X7R/NLRP3 signal. A deeper mechanical study indicated that an overexpression of P2X7R further enhanced the protective effect of dioscin. Whilst, an inhibition of P2X7R abolished the protective effect of dioscin. These results suggested that dioscin protected type 2 diabetes cognitive dysfunction through, at least partially, regulating the P2X7R/NLRP3 signal pathway. Our findings further indicate the great value of dioscin on preventing type 2 diabetes cognitive dysfunction.

ADO/hypotaurine: a novel metabolic pathway contributing to glioblastoma development.

Significant advance has been made towards understanding glioblastoma metabolism through global metabolomic profiling. However, hitherto little is known about the role by which altered metabolism plays in driving the aggressive glioma phenotype. We have previously identified hypotaurine as one of the top-ranked metabolites for differentiating low- and high-grade tumors, and that there is also a strong association between the levels of intratumoral hypotaurine and expression of its biosynthetic enzyme, cysteamine (2-aminoethanethiol) dioxygenase (ADO). Using transcription profiling, we further uncovered that the ADO/hypotaurine axis targets CCL20 secretion through activating the NF-κB pathway to drive the self-renewal and maintenance of glioma 'cancer stem cells' or glioma cancer stem-like cells. Conversely, abrogating the ADO/hypotaurine axis using CRISPR/Cas9-mediated gene editing limited glioblastoma cell proliferation and self-renewal in vitro and tumor growth in vivo in an orthotopical mouse model, indicating that this metabolic pathway is a potential key therapeutic target. Collectively, our results unveil a targetable metabolic pathway, which contributes to the growth and progression of aggressive high-grade gliomas, as well as a novel predictive marker for glioblastoma diagnosis and therapy.

[Clinical analysis of sarcoidosis of ocular adnexa].

OBJECTIVE: To study the diagnosis and treatment of 17 patients with sarcoidosis in ocular adnexa. METHODS: The clinical data of 17 cases with sarcoidosis in ocular adnexa treated during 1993 and 2008 were retrospectively analyzed. All patients underwent surgical treatment, and the diagnosis was proven histopathologically. RESULTS: Among the 17 cases, 4 were male, and 13 were female. The patients' age ranged from 15 to 70 years, with a mean of 46.9 years. The lesions were located at the orbit (8 cases), lacrimal grand (5 cases) and eyelids (4 cases). Fourteen cases complained of the presence of a local mass, 2 cases complained of exophthalmos and 1 swelling of eyelids. Concurrent systemic sarcoidosis was present in 7 cases. Three cases coincided with lung sarcoidosis, 3 cases with uveitis and 1 case with dermatopathy. Angiotensin converting enzyme analysis was performed in 6 cases; 4 of them were elevated. Computer tomography was performed in 12 cases; in 11 cases it presented as moderate density parenchymatous mass, and in the remaining one it presented as hypodensity cystic mass. B scan of 5 cases showed hypoechoic parenchymatous homogeneous mass. None of 14 cases relapsed after 1 to 15 years follow-up. CONCLUSIONS: Ocular adnexal sarcoidosis usually presents as local mass and it should be included in the differential diagnosis of orbital and ocular adnexal lesions. Excision of localized mass alone could achieve satisfactory outcomes for isolated lesions, while for diffuse or systematic lesions, corticosteroid treatment should be prescribed routinely.

miR-146a-5p Plays an Oncogenic Role in NSCLC via Suppression of TRAF6.

Non-small cell lung cancer (NSCLC) is the most deadly cancer in the world due to its often delayed diagnosis. Identification of biomarkers with high sensitivity, specificity, and accessibility for early detection, such as circulating microRNAs, is therefore of utmost importance. In the present study, we identified a significantly higher expression of miR-146a-5p in the serum and tissue samples of NSCLC patients than that of the healthy controls. In parallel, miR-146a-5p was also highly expressed in three human NSCLC adenocarcinoma-cell lines (A549, H1299, and H1975) compared to the human bronchial epithelium cell line (HBE). By dual-luciferase reporter assay and manipulation of the expressions of miR-146a-5p and its target gene, tumor necrosis factor receptor-associated factor 6 (TRAF6), we showed that the functional effects of miR-146a-5p on NSCLC cell survival and migration were mediated by direct binding to and suppression of TRAF6. Overexpression of TRAF6 sufficiently reversed miR-146a-5p-induced cancer cell proliferation, migration, and apoptosis resistance. Our data implied that miR-146a-5p/TRAF6/NF-κB-p65 axis could be a promising diagnostic marker and a therapeutic target for NSCLC.

Concept learning through deep reinforcement learning with memory-augmented neural networks.

Deep neural networks have shown superior performance in many regimes to remember familiar patterns with large amounts of data. However, the standard supervised deep learning paradigm is still limited when facing the need to learn new concepts efficiently from scarce data. In this paper, we present a memory-augmented neural network which is motivated by the process of human concept learning. The training procedure, imitating the concept formation course of human, learns how to distinguish samples from different classes and aggregate samples of the same kind. In order to better utilize the advantages originated from the human behavior, we propose a sequential process, during which the network should decide how to remember each sample at every step. In this sequential process, a stable and interactive memory serves as an important module. We validate our model in some typical one-shot learning tasks and also an exploratory outlier detection problem. In all the experiments, our model gets highly competitive to reach or outperform those strong baselines.

Anti-tumor effect of beta-elemene in glioblastoma cells depends on p38 MAPK activation.

beta-Elemene, a natural plant drug extracted from Curcuma wenyujin, has been used as an antitumor drug for different tumors, including glioblastoma. However, the mechanism of its anti-tumor effect is largely unknown. Here we report that anti-proliferation of glioblastoma cells induced by beta-elemene was dependent on p38 MAPK activation. Treatment of glioblastoma cell lines with beta-elemene, led to phosphorylation of p38 MAPK, cell-cycle arrest in G0/G1 phase and inhibition of proliferation of these cells. Inhibition of p38 MAPK reversed beta-elemene-mediated anti-proliferation effect. Furthermore, the growth of glioblastoma cell-transplanted tumors in nude mice was inhibited by intraperitoneal injection of beta-elemene. Taken together, our findings indicate that activation of p38 MAPK is critical for the anti-proliferation effect of beta-elemene and that p38 MAPK might be a putative pharmacological target for glioblastoma therapy.

[Effect of p38 MAPK on elemene-induced cell cycle arrest in C6 glioblastoma cells].

OBJECTIVE: To observe the effect of elemene on cell cycle of rat C6 glioblastoma cells. METHODS: Cell cycle analysis and expression of p38 in C6 glioblastoma cells under elemene treatment were measured by flow cytometry and Western blot. Flow cytometry and MTT assay were used to examine cell cycle and cell proliferation while C6 glioblastoma cells were pretreated with p38 inhibitor and DN-p38 plasmids. RESULTS: The fraction of C6 in the G0/G1 phase increased 11%, 6.95%, 19.57% respectively in the presence of 40, 60 and 80 microg/ml elemene. The level of phosphorylated p38 MAPK was greatly increased in a dose and time-dependent manner. Inhibition of p38 MAPK activation with SB203580 and DN-p38 blocked elemene-induced anti-proliferation effect. CONCLUSION: Elemene could induce G0/G1 cell cycle phase arrest of C6 glioblastoma cells through up-regulation of phosphorylated p38.

[Orbital solitary fibrous tumor: a clinicopathologic analysis].

OBJECTIVE: To study clinicopathologic features, histologic characteristics, differential diagnosis and the treatment of orbital solitary fibrous tumor (SFT). METHODS: Clinical, radiographic and pathologic findings of 6 cases of SFT were retrospectively analyzed. Immunohistochemistry were performed on selected samples. RESULTS: Four patients were males and 2 were females. Patients age ranged from 19- to 57-years-old. The location of the tumor was in the muscle cone (case 1 and case 5), medial (case 3), lateral (case 4), superior (case 2) and inferolateral (case 6) portion of the orbit, respectively. The presenting symptom was proptosis in 3 cases and was mass of subconjunctival or orbit margin in other 3 cases. Image examination: SFT appeared as a round (case 6 showed irregular) and well-circumscribed parenchymatous mass that could be homogenously enhanced by contrast. Histologically, SFT displayed as a mass of spindle cells in an irregular arrangement Sometime, tumor cells could be storiform or sarciniform. Mitotic figures were infrequent and usually there were 0 to 3 mitotic figures per 10 high-power fields. Hyalinization and staghornform blood vessels were frequently observed. SFT was immunoreactive for markers such as Vim, CD34 and CD99. Two cases were recurred. CONCLUSIONS: SFT is a rare orbital tumor and could be confused with other types of orbital tumors. This tumor can be diagnosed by pathological and immunocytochemical studies, these characteristics can be used to differentiate it from other types of orbital tumors.