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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.


PubMed | The Fifth Hospital of Wuhan and Wuhan Hematology Institute
Type: Journal Article | Journal: Asian Pacific journal of tropical medicine | Year: 2016

To investigate the effects of co-transfection of miR-520c-3p and miR-132 on proliferation and apoptosis of hepatocellular carcinoma Huh7.Hepatocellular carcinoma Huh7 was cultured invitro and lipidosome was used to transfect miR-520c-3p and miR-132, respectively or together. The effects of transfection of miR-520c-3p and miR-132 on proliferation and apoptosis of Huh7 were detected by CCK8 and Annexin V staining and flow cytometry, and the expression level of the targeted gene of over-expressed miR-520c-3p and miR-132 was determined by Western blot and realtime PCR.Compared with the control group, the proliferation ability of Huh7 of the single transfected and co-transfected miR-520c-3p and miR-132 decreased significantly, and the apoptosis ratio increased distinctly (P<0.05). Besides, the effect of the co-transfection group was better than that of the single transfection group. The protein levels of GPC3 (Glypican-3) and YAP (Yes-associated protein), the target genes transfected only by miR-520c-3p and miR-132, respectively, reduced obviously (P<0.05), which was similar with the co-infected cells, but cells transfected by miR-132 only showed a decrease of YAP.The co-transfection of miR-520c-3p and miR-132 can target-regulate the expression of GPC3 and YAP, enhance the exhibition effect on proliferation of hepatocellular carcinoma Huh7 and induce cell apoptosis synergistically.


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.


Li L.,The Fifth Hospital of Wuhan | Zhang J.,The Fifth Hospital of Wuhan | Pan Q.,Wuhan University of Science and Technology | Lei C.,The Fifth Hospital of Wuhan
International Journal of Clinical and Experimental Pathology | Year: 2016

Objective: To investigate the biological significance of abundant miR-23a expression in gastric cancer (GC) and its correlation with PTEN in the pathogenesis of GC migration and invasion. Methods: The human gastric cancer cell lines SGC-7901, AGS, the immortalized cell line GES-1 derived from normal gastric mucosa. Cell transfection and selection of stable cell lines and the gene and protein levels of miR-23a and PTEN were examined to determine the molecular relationship between them in the pathogenesis of gastric cancer. Results: Inhibition of miR-23a effectively reduced migration and invasion of GC cell lines. Bioinformatics and luciferase reporter assay revealed that miR-23a specifically targeted the 3'-UTR of PTEN and regulated its expression. Down-regulation of PTEN enhanced migration and invasion of GC cell lines. Furthermore, in tumor tissues obtained from gastric cancer patients, the expression of miR-23a was negatively correlated with PTEN and the high expression of miR-23a combined with low expression of PTEN might serve as a risk factor for cancer patients. Besides, miR-23a-mediated suppression of PTEN led to activation of AKT/ERK pathways and epithelial-mesenchymal transition (EMT) in GC cells, and finally enhances the activity of GC cell proliferation and movement and promotes GC xenograft tumor growth in mouse models. Conclusion: Our study showed that miR-23a, by down-regulation PTEN, enhances migration and invasion in GC cells.


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.


PubMed | The Fifth Hospital of Wuhan
Type: Journal Article | Journal: International journal of molecular medicine | Year: 2016

Colorectal cancer is one of the most common malignancies. Previous studies have reported that cortactin (CTTN) is often overexpressed in tumors and is associated with metastasis and poor prognosis of patients. The abnormal expression of microRNAs (miRNAs or miRs) is closely related to the development and progression of various types of cancer, including colorectal cancer. However, little is known about the miRNAs targeting cortactin. In the present study, prediction using biological software revealed that cortactin has binding sites for miR-542-3p. Transfection with miR-542-3p mimic demonstrated that miR542-3p reduced the expression of cortactin in colorectal cancer cells. Dual luciferase reporter assays further demonstrated that miR-542-3p regulated cortactin in a targeted manner and that miR-542-3p expression was significantly downregulated in colorectal cancer cells. A cell proliferation assay and Transwell migration assay were undertaken: we noted that miR542-3p inhibited the proliferation and invasion of colorectal cancer cells while promoting their apoptosis. By contrast, cortactin acted antagonistically. When co-transfected with miR-542-3p mimic and CTTN overexpression vector, the inhibitory effect of miR-542-3p was blocked. This indicates that miR-542-3p regulates CTTN in a targeted manner to modulate the growth and invasion of colorectal cancer cells. The present study thus provides new targets for the prevention and treatment of colorectal cancer.

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