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Xu W.,Chongqing Medical University | Wang Y.,Chongqing Medical University | Song J.,Chongqing Medical University | Mo L.,Dazu District Peoples Hospital | Jiang T.,Chongqing Medical University
Surgical Endoscopy and Other Interventional Techniques | Year: 2016

Objective: To further understand the effects of video-assisted thoracic surgery (VATS) with one-port versus three-port VATS for primary spontaneous pneumothorax (PSP). Methods: In this study, we searched information from the PubMed, Cochrane Library, Embase, ScienceDirect, Web of Science, China National Knowledge Infrastructure (CNKI), and Wanfang Data databases from inception to September 2015 to collect data of randomized controlled trials (RCTs) and cohort studies about one-port VATS versus three-port VATS for PSP. Two independent authors were committed to screen literature, extract data, and assess the risk of bias of related studies. Then, we used the RevMan 5.20 software for a meta-analysis of one-port VATS versus three-port VATS for PSP. Results: Six cohort studies involving 310 patients were finally selected in this meta-analysis. The results of our study indicate that one-port VATS had a shorter hospital stay (SMD = −0.39, 95 % CI −0.69 to 0.09, P = 0.01), lower VAS score of 24-h post-operative pain (SMD = −0.78, 95 % CI −1.40 to −0.52, P < 0.00001), shorter chest drainage time (SMD = −0.68, 95 % CI −1.15 to −0.22, P = 0.004), and lower incidence of post-operative paraesthesia (OR = 0.13, 95 % CI 0.06 to 0.29, P < 0.00001) compared with three-port VATS. However, one-port VATS had a lower patient satisfaction score at 24 h (SMD = −0.65, 95 % CI −0.95 to −0.35, P < 0.0001) and 48 h (SMD = −0.46, 95 % CI −0.71 to −0.21, P = 0.0002). No differences in the recurrence of pneumothorax (OR = 0.58, 95 % CI 0.20 to 1.67, P = 0.32), the operation time (SMD = 1.01, 95 % CI −4.63 to 2.60, P = 0.58), and the satisfaction score at 72 h (SMD = −0.11, 95 % CI −0.44 to 0.22, P < 0.00001) were noted between the groups. Conclusion: Current evidence suggests that one-port VATS may have certain advantages over three-port VATS for PSP. More large-scale and high-quality studies are needed for authentication. © 2016 Springer Science+Business Media New York Source


Jiang L.,Chongqing Medical University | Wang P.,Dazu District Peoples Hospital | Chen H.,Chongqing Medical University
Upsala Journal of Medical Sciences | Year: 2014

Background. The forkhead box M1 (FOXM1) transcription factor plays an important role in the metastases of many cancers. Down-regulation of FOXM1 by its inhibitor, thiostrepton, can inhibit the metastatic potential of some cancers; however, there are few studies regarding the functional signicance of FOXM1 and thiostrepton in the metastases of nasopharyngeal carcinoma (NPC) and the underlying mechanism.Methods. Expression of FOXM1 in NPC, normal nasopharyngeal tissues, a NPC cell line (C666-1), and a nasopharyngeal epithelial cell line (NP69) was investigated by immunohistochemical staining, qRT-PCR, and Western blot. The correlation between FOXM1 expression and the clinical characteristics of patients was analyzed. Moreover, the effects of thiostrepton on expression of FOXM1 in C666-1 and NP69 cells, and the invasion and migration ability of C666-1 cells were examined. The expressions of MMP-2, MMP-9, fascin-1, ezrin, and paxillin were determined after treatment with thiostrepton.Results. FOXM1 was overexpressed in NPC and C666-1 cells compared with normal nasopharyngeal tissues and NP69 cells. Overexpression of FOXM1 was associated with lymph node metastasis and advanced tumor stage. Moreover, thiostrepton inhibited expression of FOXM1 in C666-1 cells in a dose-dependent manner, but had a minimal effect on NP69 cells. Thiostrepton inhibited the migration and invasion ability of C666-1 cells by down-regulating the expression of MMP-2, MMP-9, fascin-1, and paxillin.Conclusions. Overexpression of FOXM1 is associated with metastases of NPC patients. Thiostrepton inhibits the metastatic ability of NPC cells by down-regulating the expression of FOXM1, MMP-2, MMP-9, fascin-1, and paxillin. © 2014 Informa Healthcare. Source


Jiang L.,Chongqing Medical University | Wu X.,Chongqing Medical University | Wang P.,Dazu District Peoples Hospital | Wen T.,Chongqing Medical University | And 3 more authors.
Journal of Cancer Research and Clinical Oncology | Year: 2015

Purpose: We have previously reported that forkhead box M1 (FoxM1) transcription factor was overexpressed in laryngeal squamous cell carcinoma (LSCC) and was associated with development of LSCC. However, there are limited studies regarding the functional significance of FoxM1 and FoxM1 inhibitor thiostrepton in LSCC. Therefore, the aim of this study was to examine both in vitro and in vivo activity of FoxM1 inhibitor thiostrepton against LSCC cell line and nude mice.Methods: Cell viability was studied by CCK-8 assay. Cell growth was evaluated by CFSE staining and cell cycle analysis. Apoptosis was measured by flow cytometry. The mRNA and protein expression were detected by quantitative real-time RT-PCR, Western blot and immunohistochemical staining. Xenograft model of tumor formation was used to investigate how thiostrepton influences tumorigenesis in vivo.Results: Overexpression of FoxM1 in LSCC cells was down-regulated by thiostrepton in a dose-dependent manner. Thiostrepton caused dose- and time-dependent suppression of cell viability of LSCC. Moreover, thiostrepton induced cell cycle arrest at S phase at early time and inhibited DNA synthesis in LSCC cells in a dose- and time-dependent manner by down-regulation of cyclin D1 and cyclin E1. Thiostrepton also induced dose- and time-dependent apoptosis of LSCC cells by down-regulation of Bcl-2, up-regulation of Bax and p53, and inducing release of cytochrome c accompanied by activation of cleaved caspase-9, cleaved caspase-3 and cleaved PARP. In addition, z-VAD-fmk, a universal inhibitor of caspases, prevented activation of cleavage caspase-3 and abrogates cell death induced by thiostrepton treatment. Furthermore, FADD and cleaved caspase-8 were activated, and expression of cIAP1, XIAP and survivin were inhibited by thiostrepton. Finally, treatment of LSCC cell line xenografts with thiostrepton resulted in tumorigenesis inhibition of tumors in nude mice by reducing proliferation and inducing apoptosis of LSCC cells.Conclusions: Collectively, our finding suggest that targeting FoxM1 by thiostrepton inhibit growth and induce apoptosis of LSCC through mitochondrial- and caspase-dependent intrinsic pathway and Fas-dependent extrinsic pathway as well as IAP family. Thiostrepton may represent a novel lead compound for targeted therapy of LSCC. © 2014, Springer-Verlag Berlin Heidelberg. Source


Jiang L.,Chongqing Medical University | Wang P.,Dazu District Peoples Hospital | Chen L.,Chongqing Medical University | Chen H.,Chongqing Medical University
International Journal of Clinical and Experimental Pathology | Year: 2014

Nasopharyngeal carcinoma (NPC) is a head and neck malignant tumor rare throughout most of the world but common in Southern China. Forkhead box M1 (FoxM1) transcription factor has been shown to play important role in the development and progression of human cancers. We have previously found that FoxM1 was overexpressed in NPC patients and was associated with development of NPC. However, the exact functional significance of FoxM1 and its inhibitor thiostrepton in NPC is little known. The purpose of this study was to investigate in vitro activity of down-regulation of FoxM1 by thiostrepton or siRNA against NPC cell line. FoxM1 inhibition by thiostrepton or siRNA inhibited proliferation of NPC cells by down-regulation of cyclin D1 and cyclin E1. Transformation ability of NPC cells was suppressed by thiostrepton. FoxM1 inhibition by thiostrepton induced apoptosis of NPC cells by down-regulation of bcl-2, up-regulation of bax and p53, and inducing release of cytochrome c accompanied by activation of caspase-9, cleaved caspase-3 and cleaved PARP. In addition, FoxM1 inhibition by siRNA transfection also down-regulated expression of bcl-2 and up-regulated expression of bax, p53, cleaved caspase-3 and cleaved PARP. Furthermore, FADD and cleaved caspase-8 expression were up-regulated by thiostrepton or FoxM1 siRNA, and expression of cIAP1 and XIAP was inhibited by thiostrepton. At last, FoxM1 inhibition by thiostrepton reduced the expression of HIF-1α and VEGF, and transfection of FoxM1 siRNA decreased VEGF expression but not HIF-1α. Collectively, our finding suggest that FoxM1 inhibition by thiostrepton or siRNA suppresses proliferation, transformation ability, angiogenesis, and induces apoptosis of NPC. Source


Hu T.,Dazu District Peoples Hospital | Qin C.,Dazu District Peoples Hospital | Wang J.,Dazu District Peoples Hospital | You Y.,Dazu District Peoples Hospital
Tumor Biology | Year: 2015

Malignant glioma is the most common type of primary brain tumor and represents one of the most aggressive and lethal human cancer types. Glioma recurrence is a common event; however, the relevant molecular mechanisms in this setting are not well-understood. In this study, we investigated glucose-regulated protein 94 (GRP94) expressions in human glioma and aimed to determine the roles of GRP94 expression affects cell proliferation, invasion, and regulatory signaling in human glioma U87 cells. Our results showed that GRP94 was overexpressed at both mRNA and protein levels in high-grade glioblastoma as compared with normal brain tissues. High GRP94 levels also predict shorter overall survival of glioma patients. RNAi-mediated silencing of GRP94 suppressed cellular proliferation, colony formation ability in glioma cells. Depletion of GRP94 also inhibited cell migration and invasion ability in glioma cell. Furthermore, gene microarray analysis revealed that GRP94 depletion caused the dysregulation of critical pathway, Wnt/β-catenin signaling pathway. We next demonstrated GRP94 regulates Wnt/β-catenin signaling pathway to promote the proliferation of glioblastoma cells. Conclusion, our findings establish GRP94 as progression markers and druggable targets in glioblastoma, relating their oncogenic effects to activation of the Wnt/β-catenin signaling pathway. © 2015, International Society of Oncology and BioMarkers (ISOBM). Source

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