Educational experience of male students in a baccalaureate nursing program in China.

Hampered by culture norms and social values, the proportion of male nursing students in China is low. Their learning experience will add weight to culturally valid nursing education. This study explored Chinese male nursing students' educational experience in a baccalaureate nursing program. A qualitative approach was used, with a purposive sample of 14 participants. Data were collected through semi-structured interviews and analyzed for thematic content. Four theme clusters emerged from the findings: choosing nursing as a career, challenges to studying nursing by gender, dilemma to nursing profession and personal benefits of studying nursing. Most of the participants passively chose nursing major. The data provided evidence that Chinese culture hindered male engaged in nursing. Low admission scores of nursing in NCEE provide an opportunity to recruit male student. Positive aspects of gender neutral portrayal of nursing help to recruit more male nursing students.

Scutellarin inhibits the metastasis and cisplatin resistance in glioma cells.

BACKGROUND: Scutellarin is a natural flavone compound that possesses anti-tumor and chemosensitization effects in several cancers. However, the effects of scutellarin on metastasis and chemoresistance in glioma have not been illustrated. METHODS: Glioma cells were treated with scutellarin in the presence or absence of LY294002. Cell proliferation was measured using a Cell Proliferation BrdU ELISA kit. Cell migration and invasion were analyzed using transwell assay. The expressions of E-cadherin, N-cadherin, vimentin, p-PI3K, PI3K, p-AKT, AKT, p-mTOR and mTOR were measured using Western blot. Furthermore, cells were incubated in the presence of cisplatin with or without the pretreatment of scutellarin. Cell viability was detected by the MTT assay. Cell apoptosis was measured using a histone/DNA ELISA detection kit. The expressions of ABCB1 and ABCG2 were detected using Western blot. RESULTS: In the present study, we found that scutellarin inhibited the proliferation, migration, and invasion of glioma cells. Scutellarin induced E-cadherin expression and reduced the expressions of N-cadherin, and vimentin in glioma cells. Our results also revealed that scutellarin enhanced chemosensitivity to cisplatin, as evidenced by the decreased cell viability to cisplatin and induced cell apoptosis. Moreover, scutellarin inhibited the expressions of ATP-binding cassette subfamily B member 1 and ATP-binding cassette sub-family G member 2 in cisplatin-resistant glioma cells. Scutellarin also prevented the activation of phosphatidylinositol 3-kinase/Akt/mammalian target of rapamycin pathway. CONCLUSION: The data suggested that scutellarin suppressed metastasis and chemoresistance in glioma cells. Scutellarin might be a new therapeutic approach for the glioma therapy.

A calcium sensor calcineurin B-like 9 negatively regulates cold tolerance via calcium signaling in Arabidopsis thaliana.

Calcineurin B-like protein 9 (CBL9) plays important roles in response to ABA, K+ deprivation in plants. However, whether CBL9 modulates plant adaptation to low-temperature stress is elusive. In this study, we demonstrated that the cbl9 mutants increased freezing tolerance under both cold-acclimating and nonacclimating conditions in Arabidopsis. Cold-induced changes of cytosolic free calcium concentration ([Ca2+]cyt) were then monitored by aequorin-expressed Arabidopsis plants. The results showed that the cold-triggered increases in [Ca2+]cyt levels in cbl9 mutants were clearly higher than those in wild type (WT) plants, while cold-affected changes in free calcium concentration within cytosolic microdomains adjacent to the vacuolar membrane ([Ca2+]md) in cbl9 mutants were similar to those in WT plants. In addition, treatments of seedlings with Ca2+ chelator ethylene glycol-bis(2-aminoethylether)-N,N,N',N'-tetraacetic acid (EGTA) and Ca2+ channel blocker lanthanum chloride markedly inhibit changes of [Ca2+]cyt in cbl9 mutants, while the inhibition of calcium release by lithium chloride from intracellular pools demonstrated consistent suppression of [Ca2+]cyt in cbl9 mutants and WT plants. Together, these results indicate that CBL9 negatively modulates cold tolerance through decreasing [Ca2+]cyt in Arabidopsis.

Retracted Article: PKM2 overexpression protects against 6-hydroxydopamine-induced cell injury in the PC12 cell model of Parkinson's disease via regulation of the brahma-related gene 1/STAT3 pathway.

According to published estimates, pyruvate kinase isoform M2 (PKM2) was expressed in low amounts in patients with Parkinson's disease (PD). However, the function and molecular mechanism of PKM2 in PD remain largely unknown. The main purpose of our study was to reveal the function and mechanism of PKM2 in the in vitro model of PD. Here, we show that PKM2 decreased in PC12 cells after 6-hydroxydopamine (6-OHDA) treatment, which inhibited PC12 cell survival and induced its apoptosis. PKM2 overexpression is required for 6-OHDA-induced PC12 cell survival. Moreover, up-regulated PKM2 expression suppressed PC12 cell apoptosis and caspase-3 activity compared with the 6-OHDA treatment alone group. Increased brahma-related gene 1 (Brg1) and p-STAT3 expression was observed in PKM2-overexpressed PC12 cells compared to those in 6-OHDA treated PC12 cells. Further studies suggested that Brg1 knockdown impeded the high expression of p-STAT3, which was induced by PKM2 overexpression. Finally, the STAT3 inhibitor reversed the effects of PKM2 on cell survival and apoptosis in 6-OHDA-induced PC12 cells. Our results suggest that PKM2 was involved in 6-OHDA-induced PC12 cell injury by mediating the Brg1/STAT3 pathway.

Raf kinase inhibitor protein protects microglial cells against 1-methyl-4-phenylpyridinium-induced neuroinflammation in vitro.

The Raf kinase inhibitor protein (RKIP), belonging to a member of the phosphatidylethanolamine-binding protein (PEBP) family, is involved in regulating neural development. However, the role of RKIP in microglial cells stimulated with 1-methyl-4-phenylpyridinium (MPP+) has not been determined. Thus, in the present study, we investigated the role of RKIP and its underlying mechanism in Parkinson's disease (PD). Our results showed that the expression of RKIP was significantly reduced in BV-2 cells treated with MPP+. Overexpression of RKIP markedly rescued cell viability and inhibited cell apoptosis in BV-2 cells exposed to MPP+. In addition, overexpression of RKIP inhibited MPP+-induced the production of pro-inflammatory molecules in BV-2 cells. Similar results were observed in primary microglial cells isolated from neonatal mice. Exploration of the underlying mechanisms of its action indicated that overexpression of RKIP prevented the activation of NF-κB and MEK/ERK pathways in MPP+-stimulated BV-2 cells. Taken together, these findings indicated that RKIP suppresses apoptosis and inflammation in MPP+-treated microglial cells through the inactivation of NF-κB and MEK/ERK signaling pathways. Thus, RKIP may be a promising target molecular involving in the pathogenesis of PD.

Knockdown of TRIM37 suppresses the proliferation, migration and invasion of glioma cells through the inactivation of PI3K/Akt signaling pathway.

Tripartite motif 37 (TRIM37), a member of the TRIM protein family, was involved in the tumorigenesis of several types of cancer. However, the expression pattern and role of TRIM37 in glioma remain unclear. Therefore, the aim of the present study was to investigate the role of TRIM37 in glioma, and to determine the molecular mechanisms. Our results demonstrated that TRIM37 was highly expressed in human glioma tissues and cell liens. Additionally, knockdown of TRIM37 dramatically inhibited the proliferation, migration/invasion, and the epithelial-mesenchymal transition (EMT) phenotype in glioma cells. Furthermore, knockdown of TRIM37 significantly reduced the levels of phosphorylated PI3K and Akt in U87MG cells, and an activator of PI3K/Akt signaling (SC79) partly reversed the inhibitory effects of si-TRIM37 on glioma cell proliferation and migration. Taken together, our results demonstrated that TRIM37 functions as an oncogene in the development and progression of glioma. TRIM37 knockdown inhibited the proliferation and invasion of human glioma cells at least in part through the inactivation of PI3K/Akt signaling pathway.

Retracted Article: TRIM22 functions as an oncogene in gliomas through regulating the Wnt/ß-catenin signaling pathway.

The tripartite motif-containing (TRIM) family is a group of proteins that are implicated in a plethora of pathological conditions. TRIM22 has been found to be involved in various cancers; however, the role of TRIM22 in gliomas has not been reported. The present study aimed to evaluate the expression pattern of TRIM22 and its function in gliomas. TRIM22 expressions in glioma tissues and cell lines were measured by RT-PCR and western blot analysis. To knockdown TRIM22 by small hairpin RNAs (shTRIM22), the U118 cells were transfected with pLKO.1-shTRIM22 plasmid or pLKO.1 plasmid. Cell proliferation was measured using CCK-8 assay. Transwell assays were performed to evaluate the migration and invasion. The epithelial-mesenchymal transition (EMT) was assessed by detecting the expressions of E-cadherin, N-cadherin and vimentin with western blot analysis. A xenograft mouse model was established to evaluate the effect of TRIM22 silencing on tumor growth in vivo. The expressions of ß-catenin, cyclin D1, and c-Myc were analyzed by western blot analysis. TRIM22 was significantly overexpressed in glioma tissues and cell lines. In vitro studies demonstrated that TRIM22 knockdown inhibited cell proliferation, migration, and invasion. Additionally, TRIM22 silencing increased the expressions of E-cadherin, and decreased the expressions of N-cadherin and vimentin. Nude mouse xenograft assay showed that TRIM22 silencing inhibited tumor growth in vivo. Furthermore, silencing of TRIM22 inhibited the activation of the Wnt/ß-catenin pathway. Treatment with LiCl, an activator of the Wnt/ß-catenin pathway, attenuated the effects of shTRIM22 on U118 cells. Silencing of TRIM22 inhibited proliferation, migration and invasion, as well as repressing the EMT process in glioma cells. The Wnt/ß-catenin pathway was involved in the effect of TRIM22.

PAQR3 inhibits the proliferation, migration and invasion in human glioma cells.

Progestin and AdipoQ Receptor 3 (PAQR3), a member of the PAQR family, is down-regulated in several types of cancers and has been closely associated with tumor progression and development. However, little is known about the functions of PAQR3 in the tumorigenesis of human glioma. Therefore, in this report, we investigated the role of PAQR3 in human glioma. Our results showed that the expression of PAQR3 was significantly reduced in human glioma tissues and cell lines. PAQR3 overexpression inhibited the proliferation of glioma cells in vitro and attenuated tumor xenograft growth in vivo. In addition, PAQR3 overexpression suppressed the migration and invasion of glioma cells, as well as prevented the EMT process. Mechanistic studies demonstrated that PAQR3 overexpression significantly down-regulated the levels of phosphorylated PI3K and Akt in U251 cells. In conclusion, these results demonstrated that PAQR3 inhibited the proliferation, migration and invasion in glioma cells, at least in part, through the inactivation of PI3K/Akt signaling pathway. Therefore, PAQR3 may be a therapeutic target for the treatment of glioma.

Wnt/ß-catenin up-regulates Midkine expression in glioma cells.

Midkine, also known as neurite growth-promoting factor 2 (NEGF2), plays an important role in cell proliferation, apoptosis and differentiation. Recent studies have shown that Midkine is up-regulated in several types of human cancers. However, the molecular mechanism for its up-regulation remains poorly understood. Activation of Wnt/ß-catenin signaling is viewed as crucial for multiple tumor growth and metastasis, including glioma. In the present study, we found that Wnt3a administration or transfection of a constitutively activated ß-catenin promoted Midkine expression in glioma cells. We further identified a TCF/LEF binding site, with which beta-catenin interacts, on the proximal promoter region of Midkine gene, by luciferase reporter and chromatin immunoprecipitation assays. Thus, our results suggest a previously unknown Wnt/ß-catenin/Midkine molecular network controlling glioma development.

MicroRNA-214 targets PCBP2 to suppress the proliferation and growth of glioma cells.

PCBP2, a member of the poly(C)-binding protein (PCBP) family, is involved in posttranscriptional and translational regulation by interacting with single-stranded poly(C) motifs in target mRNAs. Recent studies have shown that PCBP2 is overexpressed and plays an important role in human cancers, including glioma. However, the molecular basis for its up-regulation remains poorly understood. Here, we show that microRNA-214 (miR-214) interacts with the 3'-untranslated region of PCBP2 mRNA and induces its degradation, leading to reductions in its protein expression. As a result, overexpression of miR-214 mimics significantly inhibited, while its antisense oligos proliferation and growth of glioma cells. Restoration of PCBP2 remarkably reversed the tumor-suppressive effects of miR-214 on cell proliferation and growth. In summary, our data indicate that miR-214 may function as tumor suppressor in glioma by targeting PCBP2.