The Fifth Hospital of Wuhan

Wuhan, China

The Fifth Hospital of Wuhan

Wuhan, China
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Tong W.,The Fifth Hospital of Wuhan | Yang L.,Hubei Cancer Hospital | Yao J.,Chinese PLA General Hospital | He A.,The Fifth Hospital of Wuhan
OncoTargets and Therapy | Year: 2017

At present, a large number of long noncoding RNAs (lncRNAs) from the human genome have been discovered. Meanwhile, emerging evidence has indicated that lncRNAs could play a critical role in the regulation of cellular processes such as cancer progression and metastasis. However, the functions of some new lncRNAs in the complex transcriptional process are mostly unknown at present. Existing studies suggest that loss of WW domain-containing oxidoreductase (WWOX) expression is linked with poor prognosis in numerous cancers, including epithelial ovarian cancer (EOC). However, the functional role of its antisense transcript RP11-190D6.2 is not clear to date. In this study, WWOX antisense transcript RP11-190D6.2 was analyzed specifically in EOC cells using real-time polymerase chain reaction and gain-/ loss-of-function studies. We found that RP11-190D6.2 expression was positively correlated with WWOX expression. The RP11-190D6.2 expression was markedly downregulated in tumor tissues compared with normal tissues, but the RP11-190D6.2 expression was significantly downregulated in four EOC cell lines compared with human ovarian surface epithelial cell line. RP11-190D6.2 overexpression resulted in the increase of WWOX expression, whereas its knockdown led to the decrease of WWOX expression. We also found that RP11-190D6.2 was restored by 5-aza-2′-deoxycytidine treatment in EOC. In addition, the RP11-190D6.2 overexpression and knockdown experiments revealed that RP11-190D6.2 overexpression inhibited proliferation, migration, and invasion abilities in HO8910-PM cells, whereas RP11-190D6.2 knockdown in HEY-A8 cells had the opposite effect. The analyses in EOC implicate that RP11-190D6.2 may play a pivotal role in the regulation of tumor metastasis, suggesting that RP11-190D6.2 may serve as a potential biomarker and therapeutic target for EOC. © 2017 Tong et al.

Cao D.-D.,Renmin University of China | Xu H.-L.,The Fifth Hospital of WuHan | Liu L.,Fudan University | Zheng Y.-F.,Renmin University of China | And 3 more authors.
Oncotarget | Year: 2017

Objective: Transcatheter arterial chemoembolization (TACE) and thalidomide have been used for treating primary hepatocellular carcinoma(HCC). This study aims to evaluate the clinical efficacy and safety of thalidomide and TACE in primary HCC. Methods: Randomized controlled trials(RCTs) about efficacy and safety of thalidomide combined with TACE for primary HCC were identified from the Cochrane Library, Pubmed, Embase, CNKI, and Wan Fang until August, 2016. The retrieved trials were reviewed and the data were extracted by two reviewers, independently. Combined analyses of survival rates, overall response rate(ORR), disease control rate(DCR), changes of KPS, parameters of cellular immunity and vascular endothelial growth factor(VEGF), and adverse events were performed using RevMan 5.3 software. Results: A total of 23 RCTs involving 1836 patients were included. The results showed that thalidomide plus TACE was significantly superior in increasing 6-month survival rate(OR = 1.79, 95% CI:1.02-3.15, P = 0.04), 1-year survival rate(OR = 1.76, 95% CI:1.38-2.24, P < 0.0001), 1.5-year survival rate(OR = 4.72, 95% CI:2.64-8.43, P < 0.001), 2-year survival rate(OR = 1.78, 95% CI:1.37-2.30, P < 0.001), ORR(OR = 1.89, 95% CI:1.48-2.42, P < 0.0001), DCR(OR = 2.62, 95% CI:1.90-3.63, P < 0.001), improvement in cellular immunity(MD = 0.63, 95% CI:0.45-0.80, P < 0.0001), and reduction of VEGF(MD = -119.71, 95% CI:-135.75-103.68, P < 0.0001), when compared with TACE group. The incidences of gastrointestinal reactions, myelosuppression, and liver dysfunction were similar between combination group and TACE group(P > 0.05). However, compared to TACE, the combination of thalidomide and TACE had a higher incidence of drug rash(OR = 6.35, 95% CI:2.75-14.68, P < 0.0001). Conclusion: Our findings suggest that thalidomide combined with TACE shows better clinical efficacy and tolerable adverse events in patients with primary HCC when compared with TACE alone. © Cao et al.

Cao D.,Renmin University of China | Xu H.,The Fifth Hospital of Wuhan | Xu M.,Renmin University of China | Qian X.,Renmin University of China | And 2 more authors.
Oncotarget | Year: 2017

Objective: To systematically evaluate the clinical efficacy of glutamine in treating radiation enteritis in cancer patients treated with radiotherapy. Methods: Electronic databases including Pubmed, Embase, the Cochrane library, and CNKI were systematically searched, until April 2016. Randomized controlled trials (RCT) of glutamine in the treatment of radiation enteritis in cancer patients were searched, and RevMan 5.3 software was used for Meta-analysis. Results: A total of 13 RCTs were included, involving 979 patients. The results of meta-analysis showed that the total efficacy of glutamine was higher for patients with radiation enteritis compared with that in control group, however, there was no statistically significant difference(OR = 3.07, 95%CI: 0.79-11.96; P > 0.05). The combined ORs for all 5 grades(from grade 0 to grade 4) of radiation enteritis in patients receiving glutamine were 2.06, 1.35, 0.55, 0.62 and 0.59, respectively(P > 0.05 for all). Glutamine also failed to significantly improve the symptoms of radiation enteritis in terms of tenesmus, abdominal cramping and blood in bowel movement(P > 0.05). Conclusions: Implementation of glutamine fails to improve the severity and symptoms in patients with radiation enteritis.

Pang E.-J.,Shanghai JiaoTong University | Pang E.-J.,The Fifth Hospital of Wuhan | Pang E.-J.,Dalian Medical University | Yang R.,Shanghai JiaoTong University | And 8 more authors.
Tumor Biology | Year: 2015

Long non-coding RNAs (lncRNAs) have been proved to serve as a critical role in cancer development and progression. However, little is known about the pathological role of lncRNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) in pancreatic cancer patients. The aims of this study are to measure the expression of lncRNA MALAT1 in pancreatic cancer patients and to explore the clinical significance of the lncRNA MALAT1. Using qRT-PCR, the expression of lncRNA MALAT1 was measured in 126 pancreatic cancer tissues and 15 adjacent non-cancerous tissues. In the present study, our results indicated that lncRNA MALAT1 was highly expressed in pancreatic cancer compared with adjacent non-cancerous tissues (P < 0.001), and positively correlated with clinical stage (early stages vs. advanced stages, P < 0.001), tumor size (<2 vs. ≥2 cm, P = 0.004), lymph node metastasis (negative vs. positive, P < 0.001), and distant metastasis (absent vs. present, P = 0.001) in pancreatic cancer patients. Furthermore, we also found that lncRNA MALAT1 overexpression was an unfavorable prognostic factor in pancreatic cancer patients (P < 0.001), regardless of clinical stage, tumor size, lymph node metastasis, and distant metastasis. Finally, increased lncRNA MALAT1 expression was an independent poor prognostic factor for pancreatic patients through multivariate analysis (P = 0.018). In conclusion, overexpression of lncRNA MALAT1 serves as an unfavorable prognostic biomarker in pancreatic cancer patients. © 2014, International Society of Oncology and BioMarkers (ISOBM).

Ji M.,Renmin University of China | Yuan L.,Criminal Science and Technology Studio | Lv X.,Renmin University of China | Dong W.,Renmin University of China | Peng X.,The Fifth Hospital of Wuhan
Experimental and Therapeutic Medicine | Year: 2014

Increasing evidence has demonstrated that ezrin-radixin-moesin (ERM)-binding phosphoprotein 50 (EBP50) is involved in the malignant transformation of numerous human cancers. The present study investigated the involvement of EBP50 overexpression in the tumorigenicity of pancreatic cancer (PC). The results revealed that overexpression of EBP50 suppressed cell growth, promoted cell apoptosis and arrested G1-to-S phase progression in two human PC cell lines. Overexpression of EBP50 also suppressed B-cell lymphoma 2 (Bcl-2) expression. Furthermore, nude mouse tumor xenograft models were established by the subcutaneous injection of cell lines stably transfected with an EBP50-expressing plasmid. The in vivo data indicated that overexpression of EBP50 inhibited the growth of the PC tumors and induced cell apoptosis. Thus, the present study demonstrated that EBP50 overexpression induces growth inhibition and apoptosis in PC by decreasing Bcl-2 expression. The results suggest that EBP50 may function as a potential tumor suppressor in vivo and in vitro.

PubMed | the Fifth Hospital of Wuhan, Hubei Provincial Hospital of TCM, Peking Union Medical College, Chinese Institute of Basic Medical Sciences and Huazhong University of Science and Technology
Type: Journal Article | Journal: Cell research | Year: 2016

Developing novel approaches to reverse the drug resistance of tumor-repopulating cells (TRCs) or stem cell-like cancer cells is an urgent clinical need to improve outcomes of cancer patients. Here we show an innovative approach that reverses drug resistance of TRCs using tumor cell-derived microparticles (T-MPs) containing anti-tumor drugs. TRCs, by virtue of being more deformable than differentiated cancer cells, preferentially take up T-MPs that release anti-tumor drugs after entering cells, which in turn lead to death of TRCs. The underlying mechanisms include interfering with drug efflux and promoting nuclear entry of the drugs. Our findings demonstrate the importance of tumor cell softness in uptake of T-MPs and effectiveness of a novel approach in reversing drug resistance of TRCs with promising clinical applications.

Gao L.,University of Newcastle | Xia L.,Renmin University of China | Pan S.-Q.,Renmin University of China | Xiong T.,The Fifth Hospital of Wuhan | Li S.-C.,University of Newcastle
Epilepsy and Behavior | Year: 2014

Objectives: This study aimed to translate and validate the Liverpool Seizure Severity Scale (LSSS) in Chinese-speaking patients with epilepsy and explore the determinants of seizure severity in China. Methods: Accepted procedures were followed to translate the LSSS. Each participant was interviewed to complete the LSSS, Seizure Severity Index, Quality of Well-being Scale Self-Administered (QWB-SA), EuroQol (EQ-5D), and Mini Mental State Examination (MMSE). Construct validity and internal consistency were assessed. The determinants of seizure severity were explored. Results: The construct validity of the LSSS was demonstrated by good convergent and discriminant validities. Cronbach's alpha and the intraclass correlation coefficient were 0.886, respectively. In the multivariate analysis, seizure types (p. = 0.001), seizure frequency (p. = 0.001), and numbers of antiepileptic drugs (p. = 0.042) predicted the scores on the LSSS. Types of antiepileptic drugs also contributed to the variation in the LSSS scores. Conclusions: Chinese LSSS is a valid, reliable, and sensitive seizure severity scale. Seizure frequency, seizure types, and quantities and types of AEDs predict seizure severity. © 2013 Elsevier Inc.

Jiang G.,Huazhong University of Science and Technology | Zhao J.,Huazhong University of Science and Technology | Xiao X.,Huazhong University of Science and Technology | Tao D.,The Fifth Hospital of Wuhan | And 5 more authors.
Cancer Letters | Year: 2011

Although the anti-cancer agent methyl jasmonate (MJ) has been shown to selectively target malignant cells while sparing normal ones, hormone-refractory prostate cancer cells are relatively resistant to MJ than other cancer cells. In the present study, we investigated the effect of cell permeable seven-residue peptide of Smac (SmacN7), an antagonist of the inhibitor of apoptosis proteins (IAPs), on MJ-induced apoptosis. SmacN7 significantly enhanced the growth inhibition effect of MJ in human prostate cancer cells, but not in proximal tubular epithelial cells. Moreover, SmacN7 sensitizes MJ-induced apoptosis through both caspase-9-dependent and -independent pathways. Thus, blockade of the over-expressed IAPs in cancer cells could yield a potential therapeutic benefit in jasmonates-based chemotherapy. © 2010 Elsevier Ireland Ltd.

Xiang W.,Huazhong University of Science and Technology | He J.,Huazhong University of Science and Technology | Huang C.,Huazhong University of Science and Technology | Chen L.,Huazhong University of Science and Technology | And 7 more authors.
Oncotarget | Year: 2015

Inactivation of human SET domain containing protein 2 (SETD2) is a common event in clear cell renal cell carcinoma (ccRCC). However, the mechanism underlying loss of SETD2 function, particularly the post-transcriptional regulatory mechanism, still remains unclear. In the present study, we found that SETD2 was downregulated and inversely correlated with high expression of miR-106b-5p in ccRCC tissues and cell lines. Over-expression of miR-106b-5p resulted in the decreased mRNA and protein levels of SETD2 in ccRCC cells. In an SETD2 3'-UTR luciferase reporter system, miR-106b-5p downregulated the luciferase activity, and the effects were abolished by mutating the predicted miR-106b-5p binding site. Moreover, attenuation of miR-106b-5p induced cell cycle arrest at G0/G1 phase, suppressed cell proliferation, enhanced processing of caspase-3, and promoted cell apoptosis in ccRCC cells, whereas these effects were reversed upon knockdown of SETD2. In addition, transfection of miR-106b-5p antagomir resulted in the increased binding of H3K36me3 to the promoter of p53 and enhanced its activity, as well as upregulated the mRNA and protein levels of p53, and the effects were also abolished by cotransfection with si-SETD2. Collectively, our findings extend the knowledge about the regulation of SETD2 at the posttranscriptional level by miRNA and regulatory mechanism downstream of SETD2 in ccRCC.

PubMed | The Fifth Hospital of Wuhan, The Central Hospital of Wuhan, Zhengzhou University and Huazhong University of Science and Technology
Type: | Journal: Cancer letters | Year: 2016

Emerging evidences have indicated that long non-coding RNAs (LncRNAs) play vital roles in cancer development and progression. Previous studies have suggested that overexpression of SPRY4-IT1 predicates poor prognosis and promotes tumor progress in several cancers. However, the underlying mechanism of SPRY4-IT1 in bladder cancer remains unknown. In this study, we found that SPRY4-IT1 knockdown induced inhibition of cell proliferation, cell migration and invasion ability, and caused promotion of apoptosis in bladder cancer both invitro and invivo. Mechanistically, knockdown of SPRY4-IT1 increased the expression of miR-101-3p and subsequently inhibited the expression of EZH2 at posttranscriptional level. Importantly, SPRY4-IT1 could directly interact with miR-101-3p and down-regulation of miR-101-3p efficiently reversed the suppression of EZH2 induced by SPRY4-IT1 shRNA. Thus, SPRY4-IT1 positively regulated the expression of EZH2 through sponging miR-101-3p, and played an oncogenic role in bladder cancer progression. Together, our study elucidates the role of LncRNA SPRY4-IT1 as a miRNA sponge in bladder cancer, and sheds new light on LncRNA-directed diagnostics and therapeutics in bladder cancer.

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