Shaanxi Provincial Tumor Hospital

Fengcheng, China

Shaanxi Provincial Tumor Hospital

Fengcheng, China
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Wang H.,Xi'an Jiaotong University | Nie L.,Shaanxi Provincial Tumor Hospital | Wu L.,Shaanxi Provincial Tumor Hospital | Liu Q.,Shaanxi Provincial Tumor Hospital | Guo X.,Xi'an Jiaotong University
Biochemical and Biophysical Research Communications | Year: 2017

Metastasis is one of the most decisive factors influencing CRC patient prognosis and current studies suggest that a molecular mechanism known as EMT broadly regulates cancer metastasis. NR2F2 is a key molecule in the development of CRC, but the roles and underlying mechanisms of NR2F2 in TGF-β induced EMT in CRC remain largely unknown. In the current study, we were interested to examine the role of NR2F2 in the TGF-β-induced EMT in CRC. Here, we found NR2F2 was upregulated in CRC cells and promotes TGF-β-induced EMT in CRC. Using comparative miRNA profiling TGF-β pre-treated CRC cells in which NR2F2 had been knocked down with that of control cells, we identified miR-21 as a commonly downregulated miRNA in HT29 cells treated with TGF-β and NR2F2 siRNA, and its downregulation inhibiting migration and invasion of CRC cells. Moreover, we found NR2F2 could transcriptional activated miR-21 expression by binding to miR-21 promoter in HT29 by ChIP and luciferase assay. In the last, our data demonstrated that Smad7 was the direct target of miR-21 in CRC cells. Thus, NR2F2 could promote TGF-β-induced EMT and inhibit Smad7 expression via transactivation of miR-21, and NR2F2 may be a new common therapeutic target for CRC. © 2017 Elsevier Inc.

Zhang L.,Qingdao University | Lei J.,Xi'an Jiaotong University | Shan Y.,Xi'an Jiaotong University | Yang H.,Shaanxi Provincial Tumor Hospital | And 2 more authors.
Mini-Reviews in Medicinal Chemistry | Year: 2013

Histone deacetylases (HDACs) regulate the expression and activity of many proteins in both cancer initiation and cancer progression. HDACs are now recognized as promising targets for anticancer agent development. HDAC inhibitors (HDACIs) are emerging as promising anticancer drugs which possess tumor-selective cytotoxicity. HDACIs could promote growth arrest, differentiation, and apoptosis of cancer cells, with minimal effects on normal tissue. Research of HDACIs is now becoming an interesting field. HDACIs comprise structurally diverse anticancer agents and have been widely used in the clinic. This review describes recent progress in the development of HDACIs, especially focusing on the design strategies, novel chemical structures, biological properties and structure-activity relationships (SARs) of HDACIs. We hope it will be helpful for medicinal chemists who are interested in the discovery of anticancer agents. © 2013 Bentham Science Publishers.

Chen X.,Shaanxi Provincial Tumor Hospital | Yongqing Z.,Shaanxi Provincial Tumor Hospital | Ding H.,Shaanxi Provincial Tumor Hospital | Nie L.,Shaanxi Provincial Tumor Hospital | Chen J.,Shaanxi Provincial Tumor Hospital
Cancer Research and Clinic | Year: 2017

Objective: To study the relationship between expression of leptin and clinical pathogenesis and prognosis of stage II colorectal cancer. Methods: The clinical data of 102 patients with colorectal cancer admitted to Shaanxi Provincial Tumor Hospital between January 2005 and December 2010 was collected and statistically analyzed. The expression of leptin in postoperative colorectal cancer tissues and 40 normal colorectal tissues was detected by P-V immunohistochemical technique. Results: The expression of leptin in cancer tissues were obviously higher than that in normal tissues [59.8 % (61/102) vs. 17.5 % (7/40), χ2 - 20.605, P = 0.000]. There was no association between leptin expression level and gender, age, tumor location, pathological grading, pathological types, tumor size, invasion depth and body mass index (all P < 0.05). Cox multivariate regression analysis showed that leptin expression (P = 0.041) and adjuvant chemotherapy (P = 0.008) were independent factors affecting OS in patients with stage II colorectal cancer. The patients with positive expression of leptin could not benefit from the adjuvant chemotherapy (P = 0.259), and patients without leptin expression had improved survival when treated by adjuvant chemotherapy (P = 0.021). Conclusion: The expression of leptin in stage II colorectal cancer tissues is obviously higher than that in normal tissues. Leptin is associated with chemotherapy resistance and therapy-independent prognosis.

PubMed | Xi'an Jiaotong University, Shanxi Province Peoples Hospital and Shaanxi Provincial Tumor Hospital
Type: Journal Article | Journal: International journal of oncology | Year: 2016

Aberrant expression of microRNA-155 (miR-155) has been reported in several human cancers and is associated with prognosis of patients. However, the clinical significance of miR155 and its underlying mechanisms involved in hepatocarcinogenesis remain to be determined. In this study, we demonstrated that the expression of miR-155 was elevated in both hepatocellular carcinoma (HCC) tissues and cell lines. Clinical association analysis revealed that high expression of miR-155 was correlated with malignant clinicopathological characteristics including large tumor size, high Edmondson-Steiner grading and TNM tumor stage. Furthermore, its high expression conferred a reduced 5-year overall survival and disease-free survival of HCC patients. Gain- and loss-of function studies revealed that miR155 promoted cell cycle progression, cell proliferation and inhibited apoptosis. Mechanistically, we identified AT-rich interactive domain 2 (ARID2) as a direct downstream target and functional mediator of miR155 in HCC cells. Notably, alterations of ARID2 expression abrogated the effects of miR155 on HCC cell proliferation, cell cycle and apoptosis. Moreover, we demonstrated that Akt phosphorylation is essential for the functional roles of miR155 through altering CyclinD1 and p27, which were key components of cell cycle machinery. Finally, we disclosed that the downregulation of miR155 suppressed tumor growth of HCC by inhibiting Akt signaling pathway. In conclusion, our results indicate that miR155 promotes tumor growth of HCC by targeting ARID2-mediated Akt phosphorylation pathway, and potentially serves as a novel prognostic biomarker and therapeutic target for HCC.

Wang L.-J.,Xi'an Jiaotong University | He C.-C.,Xi'an Jiaotong University | Sui X.,Xi'an Jiaotong University | Cai M.-J.,Xi'an Jiaotong University | And 8 more authors.
Oncotarget | Year: 2015

Intrahepatic cholangiocarcinoma (ICC) constitutes the second-most common primary hepatic malignancy. MicroRNAs (miRNAs) play important roles in the pathogenesis of ICC. However, the clinical significance of miR-21 levels in ICC remains unclear. Here, we investigated the role of miR-21 in ICC and found that its expression was significantly upregulated in serum of ICC patients. Serum miR-21 levels robustly distinguished ICC patients from control subjects. Further experiments showed that inhibition of miR-21 suppressed ICC cell proliferation in vitro and tumor growth in vivo. Specifically, inhibition of miR-21 induced cell cycle arrest and apoptosis. Moreover, PTPN14 and PTEN were identified as direct and functional targets of miR- 21. Finally, we showed high expression levels of miR-21 were closely related to adverse clinical features, diminished survival, and poor prognosis in ICC patients. This study revealed functional and mechanistic links between miR-21 and tumor suppressor genes, PTPN14 and PTEN, in the pathogenesis of ICC. MiR-21 not only plays important roles in the regulation of cell proliferation and tumor growth in ICC, but is also a diagnostic and prognostic marker, and a potential therapeutic target for ICC.

Wu L.,Xi'an Jiaotong University | Wu L.,Shaanxi Provincial Tumor Hospital | Hui H.,Shaanxi Provincial Tumor Hospital | Wang L.-J.,Xi'an Jiaotong University | And 4 more authors.
Oncology Reports | Year: 2015

Accumulating evidence has demonstrated that microRNAs (miRNAs) are involved in multiple processes in cancer development and progression. miR-326 has been identified as a tumor suppressor miRNA in several types of human cancer. However, the specific function of miR-326 and its target the nin one binding protein (NOB1) in colorectal carcinoma (CRC) remains unclear. In the present study, we found that miR-326 inhibited cell proliferation, migration and invasion, and induced cell apoptosis and cell cycle arrest of CRC cells by directly targeting NOB1. Furthermore, the upregulation of miR-326 in CRC cells was revealed to be associated with a feedback loop involving downregulation of the NOB1, which mimics the phenotype induced by miR-326. Importantly, we found that the CRC patients with high expression of miR-326 or low expression of NOB1 tend to obtain a better prognosis. Thus, for the first time, we provide convincing evidence that downregulation of miR-326 inhibited tumor proliferation and tumor metastasis by directly targeting NOB1 in CRC. NOB1 and miR-326 could be potential therapeutic targets for CRC.

PubMed | Xi'an Jiaotong University and Shaanxi Provincial Tumor Hospital
Type: Journal Article | Journal: Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine | Year: 2016

Metastasis is one of the main causes of breast cancer (BCa)-related deaths in female. It has been reported that cancer stem cell played an important role in metastasis. Here we first revealed a specific role of pyruvate kinase isozymes M2 (PKM2) in the stemness of breast cancer cells. Breast cancer tissue analysis confirmed the upregulation of PKM2 in breast cancer, and high PKM2 levels were associated with poor prognosis of breast cancer patients. Holoclone assay and colony formation assay significantly elucidated the role of PKM2 in the self-renewal of breast cancer cells. Moreover, PKM2 elevated the proportion of stem cell and the ability of sphere formation in breast cancer cells. PKM2 played its functional role in stemness by regulating -catenin. Collectively, we identified critical roles of PKM2 in the stemness of breast cancer cells which may elevate the therapeutic effect on breast cancer patients.

PubMed | National Engineering Research Center for Miniaturized Detection Systems, Northwest University, China and Shaanxi Provincial Tumor Hospital
Type: Journal Article | Journal: Oncotarget | Year: 2016

Previous studies suggested that single nucleotide polymorphisms (SNPs) in epidermal growth factor receptor (EGFR) are associated with risk of glioma. However, the associations between these SNPs and glioma patient prognosis have not yet been fully investigated. Therefore, the present study was aimed to evaluate the effects of EGFR polymorphisms on the glioma patient prognosis. We retrospectively evaluated 269 glioma patients and investigated associations between EGFR SNPs and patient prognosis using Cox proportional hazard models and Kaplan-Meier curves. Univariate analysis revealed that age, gross-total resection and chemotherapy were associated with the prognosis of glioma patients (p < 0.05). In addition, four EGFR SNPs (rs11506105, rs3752651, rs1468727 and rs845552) correlated with overall survival (OS) (Log-rank p = 0.011, 0.020, 0.008, and 0.009, respectively) and progression-free survival PFS (Log-rank p = 0.026, 0.024, 0.019 and 0.009, respectively). Multivariate analysis indicated that the rs11506105 G/G genotype, the rs3752651 and rs1468727 C/C genotype and the rs845552 A/A genotype correlated inversely with OS and PFS. In addition, OS among patients with the rs730437 C/C genotype (p = 0.030) was significantly lower OS than among patients with A/A genotype. These data suggest that five EGFR SNPs (rs11506105, rs3752651, rs1468727, rs845552 and rs730437) correlated with glioma patient prognosis, and should be furthered validated in studies of ethnically diverse patients.

Yang L.Q.,The Second Affiliated Hospital Of Xian Medical University | Zhang Y.,Chinese Academy of Sciences | Sun H.F.,Shaanxi Provincial Tumor Hospital
Genetics and Molecular Research | Year: 2016

Our study aimed to investigate the role of 2 ERCC5 promoter SNPs (rs2094258 and rs751402) in the development of gastric cancer in the Chinese population. The present hospital-based case-control study consisted of 155 patients with gastric cancer and 246 healthy controls recruited between March 2012 and December 2014. Genotyping for the rs2094258 and rs751402 polymorphic sites was carried out using polymerase chain reaction-restriction fragment length polymorphism. Statistical analyses were conducted using the SPASS version 16.0 software (SPSS, Inc., Chicago, IL, USA). As determined by the chi-square test, there was a significant difference in the genotype distributions of rs751402 between patients and controls (χ2 = 6.74, P = 0.03). By unconditional logistic regression analysis, we observed that the TT genotype in rs751402 was significantly associated with increased risk to gastric cancer as compared with the CC genotype, and the adjusted OR (95%CI) was 2.17 (1.15-4.09). Moreover, subjects carrying the T allele in rs751402 had elevated risk of developing gastric cancer when compared with those carrying the C allele, with an adjusted OR value (95%CI) of 1.47 (1.09-1.99). In conclusion, we suggest that the ERCC5 rs751402 gene polymorphism may influence the susceptibility to gastric cancer in the Chinese population. © 2016 The Authors.

PubMed | Shaanxi Provincial Tumor Hospital
Type: Journal Article | Journal: Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine | Year: 2016

Sphingosine kinase 1 (SphK1) expression is elevated in various cancers and is associated with shorter survival times for patients. However, the molecular mechanism of SphK1 up-regulation in triple-negative breast cancer (TNBC) remains unclear. In this study, we assayed the expression level of SphK1 in TNBC tissues by qRT-PCR and immunohistochemistry. The level of S1P was quantified by ELISA in the serum of TNBC patients. Our results found that the levels of SphK1 and S1P were significantly increased in TNBC patients compared with normal control. Furthermore, knockdown of SphK1 with siRNA decreased TNBC cell proliferation and inhibited cell migration/invasion. These data suggest that SphK1 has an important role in TNBC and presents an attractive therapeutic target for the treatment for TNBC.

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