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| There are 37 papers published in subject: > since this site started. | |||
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| 1. Key Differential Gene Analysis between Ewing Sarcoma Cado-Es1 Cell Line Tumor Stem Cells, Non-Tumor Stem Cells, and Mesenchymal Stem Cells | |||
| Hongliang Wu,Sihang Zheng,Qun He,Yan Li | |||
| Clinical Medicine 24 March 2022 | |||
| Show/Hide Abstract | Cite this paper︱Full-text: PDF (0 B) | |||
| Abstract:Background Ewing sarcoma is a highly malignant tumor. It is of great significance to identify new biomarkers or therapeutic targets. This study aimed to analyze the differentially expressed genes between Ewing sarcoma ERG type cell line cado-es1 tumor stem cell like cells, non-tumor stem cell like cells and mesenchymal stem cells (MSC) derived from Ewing sarcoma patients, and study the key genes related to Ewing sarcoma ERG type. Methods The NCBI SRA database data ERP104460 was retrieved, and three groups of MSC cells, tumor stem cell like cells (SP group) and non-tumor stem cell like cells (nsp group) obtained from different Ewing sarcoma patients were selected. The RNA-seq data of 9 samples in each group were analyzed to screen the significantly differentially expressed genes. Pathway enrichment analysis and the protein-protein interaction network was performed, and the hub genes were screened. Results Compared with MSC group, 8286 differentially expressed genes were obtained, including 3638 up-regulated genes and 4648 down-regulated genes. There were 9097 differentially expressed genes in nsp group compared with msc group, including 4800 up-regulated genes and 4297 down regulated genes. Compared with nsp group, four differentially expressed genes were obtained, including three up-regulated genes, U2, SNORA45b and RNU2-1. One down regulated gene was MTND1P27. These differentially expressed genes are mainly involved in biological processes and biological pathways such as cell division, cell cycle and DNA replication. By GO, KEGG and protein interaction network, 10 hub genes including THBS1, POSTN, COL1A1, COL1A2, MMP2, MMP14, SPARC, DCN, SPP1 and COL3A1 were screened in sp vs msc group; 10 hub genes including THBS1, MMP2, LOX, POSTN, COL1A1, COL1A2, MMP14, SPARC, DCN and SPP1 were obtained in nsp vs msc group. The key differential genes of PPI network between sp vs msc group and nsp vs msc group were COL3A1 and LOX. Conclusion THBS1, POSTN, COL1A1, COL1A2, MMP2, MMP14, SPARC, DCN, SPP1 and COL3A1 are key hub genes in Ewing sarcoma tumor stem cell like cells; THBS1, MMP2, LOX, POSTN, COL1A1, COL1A2, MMP14, SPARC, DCN and SPP1 are key hub genes in non-tumor stem cell like cells of Ewing sarcoma. | |||
| TO cite this article:Hongliang Wu,Sihang Zheng,Qun He, et al. Key Differential Gene Analysis between Ewing Sarcoma Cado-Es1 Cell Line Tumor Stem Cells, Non-Tumor Stem Cells, and Mesenchymal Stem Cells[OL].[24 March 2022] http://en.paper.edu.cn/en_releasepaper/content/4757042 | |||
| 2. Recent Advances of Circular RNA as a Potential Diagnostic and Therapeutic Target for Osteosarcoma | |||
| Wu Hongliang,Zheng Sihang,Li Yan | |||
| Clinical Medicine 23 March 2022 | |||
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| Abstract:Osteosarcoma is the most common primary malignant bone tumor, which is prone to early metastasis and poor prognosis. The current treatment methods need to be improved. Circular RNA is a covalently blocked circular endogenous non-coding RNA, which plays an essential role in the occurrence, development, clinical diagnosis, and treatment of various diseases. Understanding its role in osteosarcoma is conducive to the early detection, diagnosis, and treatment of osteosarcoma. In this paper, we reviewed the mechanism of action of circular RNA in the occurrence and development of osteosarcoma and its clinical application in recent years. | |||
| TO cite this article:Wu Hongliang,Zheng Sihang,Li Yan. Recent Advances of Circular RNA as a Potential Diagnostic and Therapeutic Target for Osteosarcoma[OL].[23 March 2022] http://en.paper.edu.cn/en_releasepaper/content/4756972 | |||
| 3. GDPD5 Immune Inflammation-Mediated Angiogenesis and Invasion Regulation Network in Human Hepatocellular Carcinoma (HCC) by Biocomputation | |||
| XUE Shuaidong,WANG Ling,HUANG Juxiang | |||
Clinical Medicine 12 November 2018
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| Abstract:We data-analyzed and constructed the high-expression GDPD5 immune inflammation-mediated angiogenesis and invasion regulation network in human hepatocellular carcinoma (HCC) compared with low-expression (fold change≥2) no-tumor hepatitis/cirrhotic tissues (HBV or HCV infection) in GEO data set, by using integration of gene regulatory network inference method with gene ontology (GO). Our result showed that GDPD5 immune inflammation and multi-regulation upstream network BIRC5, BRCA1, CDKN3, EYA1, HOXD4, LEF1, PLA2G1B, PROK1, PTHLH, ROBO1, SCML2, REG3A activated GDPD5, and downstream GDPD5-activated CAD, CDC2, CDKN3, DKK1, E2F1, FOXM1, HMGB2, MAP2, MYCN, MYH6, NEK2, NR5A1, PROK1 in HCC. We proposed that GDPD5 activated network enhanced blood coagulation, chemotaxis, inflammatory response, interleukin-8 production, leukocyte migration, neutrophil chemotaxis, neutrophil mediated immunity, receptor mediated endocytosis, positive regulation of DNA repair, positive regulation of protein ubiquitination, as a result of inducing immune inflammation-mediated angiogenesis and invasion regulation in HCC. Our hypothesis was verified by GDPD5 regulation subnetwork containing angiogenesis, cell proliferation, transcription from RNA polymerase II promoter, transcription from RNA polymerase III promoter, Wnt receptor signaling pathway; also by GDPD5 negative regulation subnetwork including centriole replication, fatty acid biosynthesis, transcription, cell-cell adhesion, microtubule depolymerization in HCC, respectively. | |||
| TO cite this article:XUE Shuaidong,WANG Ling,HUANG Juxiang. GDPD5 Immune Inflammation-Mediated Angiogenesis and Invasion Regulation Network in Human Hepatocellular Carcinoma (HCC) by Biocomputation[OL].[12 November 2018] http://en.paper.edu.cn/en_releasepaper/content/4746448 | |||
| 4. Clinicopathological and prognostic significance of circulating tumor cells in patients with esophageal cancer : A meta-analysis | |||
| Hou Jinxuan,Zou Kun,Xu Yu | |||
Clinical Medicine 09 September 2017
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| Abstract:The aim of this meta-analysis was to assess the clinicopathological and prognostic significance of circulating tumor cells (CTCs) in patients with esophageal cancer. We searched PubMed, EMBASE, Science Citation Index Expanded, Cochrane library (from inception to October 2016) with the key words "esophageal cancer", "circulating tumor cells", "prognosis" and "peripheral blood". Hazard ratio, risk ratio, odds ratio and their 95% confidence intervals were set as effect measures. All analyses were performed by STATA 12.0. 17 studies were retrieved, CTCs positive was significant associated with poor progression-free survival (HR = 2.55; 95%CI: 2.12-3.06) and overall survival (HR = 2.46; 95%CI: 1.94-3.11). CTCs positive were also associated with high recurrence (OR=2.66; 95%CI: 1.63-4.35) and poor response of chemoradiotherapy (RR=0.80; 95%CI: 0.66-0.97). For clinicopathological characteristics, CTCs positive was significantly associated with TNM staging, depth of infiltration, regional lymph nodes metastasis, distant metastasis, lymphatic invasion and venous invasion. The meta-analysis has confirmed the significant clinicopathological and prognostic value of CTCs positive for both PFS and OS in patients with esophageal cancer. | |||
| TO cite this article:Hou Jinxuan,Zou Kun,Xu Yu. Clinicopathological and prognostic significance of circulating tumor cells in patients with esophageal cancer : A meta-analysis[OL].[ 9 September 2017] http://en.paper.edu.cn/en_releasepaper/content/4741316 | |||
| 5. Salicylate Activates AMPK, Inhibits PDGFR/mTORC1 Signaling and Proliferation in Human Glioblastoma multiforme Cell Lines | |||
| Cai Shang,Yang chuanlai,Liu Yuanyuan,Cao Cong,Tian Ye | |||
| Clinical Medicine 03 May 2017 | |||
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| Abstract:BACKGROUND & AIMS: Salicylate activates AMPK, inhibits mTORC1 signaling in some cancer cells, GBM cells have dysregulated RTK/mTOR signaling, which promotes cell survival, proliferation and tumor growth. Thus, the goal of this study was to investigate the effects of salicylate on proliferation, AMPK and RTK/mTOR signaling in human GBM cell lines. METHODS: MTT assay, colony formation assay, and flow cytometry were used to evaluate the effects of salicylate on proliferation in GBM cell lines. The effects of salicylate on AMPK and RTK/mTOR signaling in GBM cell lines were determined by the expression of PDGFR, phosphorylation of ACC, S6 and 4EBP1 via immunoblotting. Ubiquitin-like protein LC3 was used as the marker of autophagy and was examined in GBM cell lines by immunoblotting. RESULTS: Salicylate inhibited proliferation, induced apoptosis and S phase cycle arrest in GBM cell lines. Salicylate activated AMPK, down-regulated PDGFR, and reduced mTORC1 signaling by inhibiting mTORC1 substrates S6 and 4EBP1 in GBM cell lines. Salicylate also activated autophagy, which is a characterized response of the inhibition of mTORC1. CONCLUSIONS: Salicylate is a potential anti-GBM agent, and it may exert its anti-neoplasm activity by modulation of AMPK and PDGFR/mTORC1 signaling, which is pivotal for GBM progression. Our data will also serve as the basis for in vivo studies to investigate the effects of salicylate on GBM.????? | |||
| TO cite this article:Cai Shang,Yang chuanlai,Liu Yuanyuan, et al. Salicylate Activates AMPK, Inhibits PDGFR/mTORC1 Signaling and Proliferation in Human Glioblastoma multiforme Cell Lines[OL].[ 3 May 2017] http://en.paper.edu.cn/en_releasepaper/content/4731962 | |||
| 6. Co-overexpression of DNMT1 and p53 protein is associated with unfavorable prognosis in colorectal cancer | |||
| WANG Feng,JIANG Xun,SHEN Tongyi,SHI Chenzhang,LIU Zhongchen | |||
| Clinical Medicine 24 April 2017 | |||
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| Abstract:Purpose and methods: Functional interaction between DNA methyltransferase I (DNMT1) and p53 has been shown in many cancers including colorectal cancer (CRC). However, few studies have investigated the relationship between DNMT1 and p53 expression and clinicopathological parameters in CRC. Here we report a retrospective analysis that examined the clinicopathological and prognostic significance of DNMT1 and p53 expression in 161 surgically resected CRC patients from January 2003 to December 2007 by tissue microarray and immunohistochemistry. Results: DNMT1 and p53 were over-expressed in 72.7% and 62.7% of cases, respectively, and was associated with advanced tumor stage. Poor histological differentiation and neural invasion were related to patients with higher DNMT1 and p53 expression, respectively. Moreover, a positive correlation between the expression of DNMT1 and P53 was found. Combined analysis of DNMT1 and p53 expression showed that 49.1% of the tumors displayed DNMT1+/p53+ phenotype which was significantly associated with advanced tumor stage. Furthermore, although neither DNMT1 nor p53 expression individually or in combination was of independent prognostic significance, DNMT1+/p53+ phenotype is significantly correlated with a subset of patients with definitively poor prognoses. Conclusion: These data provide evidence that DNMT1 and p53 are involved in the development and progression of CRC, and may serve as biomarkers to evaluate the diagnosis, prognosis and treatment of CRC. | |||
| TO cite this article:WANG Feng,JIANG Xun,SHEN Tongyi, et al. Co-overexpression of DNMT1 and p53 protein is associated with unfavorable prognosis in colorectal cancer[OL].[24 April 2017] http://en.paper.edu.cn/en_releasepaper/content/4727055 | |||
| 7. Sarcomatoid carcinoma transformation: a rare manifestation of EGFR TKI drug resistance in a patient with lung adenocarcinoma | |||
| XU Song,LIU Renwang,LIU Xia,SHI Tao,LI Xiongfei,ZHONG Diansheng,WANG Yan,CHEN Gang,CHEN Jun | |||
| Clinical Medicine 15 April 2017
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| Abstract:Objective: Almost all EGFR-mutant lung cancers develop resistance to EGFR tyrosine kinase inhibitors (EGFR-TKIs). Several mechanisms for this acquired resistance have been identified, including development of an EGFR T790M mutation, MET amplification, hepatocyte growth factor (HGF) overexpression, loss of PTEN expression, epithelial to mesenchymal transition and transformation to small cell lung cancer. Herein, we presented a lung cancer patient with EGFR exon 19 deltion who was resistant to EGFR TKI treatment. Method: To further explore the underlying mechanisms, we performed a gene mutation profiling by next generation sequencing (NGS). Results: The mechanism of drug resistance is very rare. Some adenocarcinoama cells aquired T790M mutation in EGFR exon 20, and other adenocarcinoama cells transformed into sarcomatoid carcinoma. Conclusion: This case inspires us again the importance of tissue re-biopsy once the acquired resistance occurs after TKI consistant pressure. Sarcomatoid carcinoma transformation is a rare manifestation of EGFR TKI drug resistance in a patient with lung adenocarcinoma. | |||
| TO cite this article:XU Song,LIU Renwang,LIU Xia, et al. Sarcomatoid carcinoma transformation: a rare manifestation of EGFR TKI drug resistance in a patient with lung adenocarcinoma[OL].[15 April 2017] http://en.paper.edu.cn/en_releasepaper/content/4725568 | |||
| 8. Treatment of primary pulmonary malignant fibrous histiocytoma: case report and literature Review | |||
| XU Song,Li Xiongfei,SHI Tao,REN Fan,YANG Fan,Liu Renwang,REN Dian,DONG Shangwen,FAN Haiyang,WEI Sen,CHEN Gang,CHEN Jun | |||
| Clinical Medicine 15 April 2017 | |||
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| Abstract:Objective: Malignant fibrous histiocytoma (MFH) is an aggressive soft tissue sarcoma which can occur in various organs. However, primary MFH arising from lung is quite rare. Method: Herein we reported a case of 61-year-old male with primary pulmonary MFH and explore the underlying mechanisms by next generation sequencing. Results: Five gene mutations, including TSC2, ARID1B, CDK8, KDM5C and CASP8, were detected and the mTOR inhibitor might be an efficient treatment for this patient. In addition, we reviewed in the English literature approximately 36 case reports of primary pulmonary MFH since 1979 and summarized the clinical features and prognosis of this rare pulmonary malignant tumor.Conclusion:MFH is not sensitive to chemo- and radio-therapy. Once the diagnosis is confirmed, a complete surgical resection is necessary. Target therapy by mTOR inhibitors might be a promising treatment. | |||
| TO cite this article:XU Song,Li Xiongfei,SHI Tao, et al. Treatment of primary pulmonary malignant fibrous histiocytoma: case report and literature Review[OL].[15 April 2017] http://en.paper.edu.cn/en_releasepaper/content/4725565 | |||
| 9. Tyr23 phosphorylation of Anxa2 enhances STAT3 activation and promotes proliferation and invasion of breast cancer cells | |||
| Jie Yuan,Ruifang Niu | |||
| Clinical Medicine 27 December 2016 | |||
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| Abstract:urpose:Overexpression of Annexin A2 (Anxa2) is positively correlated with breast cancer progression, drug resistance, and poor prognosis of patients with breast cancer. Tyr23 Phosphorylation by Src-family tyrosine kinase is an important post-translational modification of Anxa2. This modification regulates the subcellular localization and functions of Anxa2 and has significant effects on cell proliferation, migration, and invasion. This study aims at revealing the association of Anxa2-Tyr23 phosphorylation in Anxa2-mediated acceleration of breast cancer progression and their elaborate molecular mechanisms. Methods:Cell biological function experiments were performed to determine the effects of Anxa2-Tyr23 Phosphorylation on breast cancer cell proliferation and invasion in vitro and metastasis in vivo. The interaction of Tyr23 phosphorylated Anxa2 and STAT3 was verified by co-immuniprecipitation assay. Related mRNA and protein expression levels ofcyclin D1 and MMP2/9 andphosphorylation level of STAT3 were detected. Results:Anxa2-Tyr23 phosphorylation is necessary for proliferation, invasion, and metastasis of breast cancer cells in vitro and in vivo. Tyr23 phosphorylated Anxa2 binds and enhances the sensitivity of STAT3 activation in response to IL-6, thereby increasing the protein and mRNA expression levels of cyclin D1 and MMP2/9which are STAT3 key target genes and serve pivotal regulatory functions in cell proliferation and invasion, respectively. Conclusion: Our findings further confirmed the regulatory role of Anxa2 and revealed the direct relationship betweenAnxa2-Tyr23 phosphorylation and activation of STAT3. Moreover, this study provides novel insights into the function of Anxa2-Tyr23 phosphorylation in signal transduction for further understanding of the mechanism through which Anxa2 promotes the progression of breast cancer.n) | |||
| TO cite this article:Jie Yuan,Ruifang Niu. Tyr23 phosphorylation of Anxa2 enhances STAT3 activation and promotes proliferation and invasion of breast cancer cells[OL].[27 December 2016] http://en.paper.edu.cn/en_releasepaper/content/4715882 | |||
| 10. No Association Between Physical Activity and Risk of Ovarian Cancer: A Meta-analysis of Observational Studies | |||
| ZHAO Jitong,ZHOU Shengtao,LIN Xiaojuan | |||
| Clinical Medicine 14 June 2016 | |||
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| Abstract:In Objective: To evaluate the association between physical activity and the risk of ovarian cancer. Methods: We searched PubMed, EMBASE and the Cochrane Library for cohort and case-control studies which examined association between physical activity and ovarian cancer risk. A meta-analysis was conducted to estimate the summary relative risk (RR). Results: A total of 23 studies (twelve cohort studies and eleven case-control studies) met the inclusion criteria. In the meta-analysis of all included studies, when compared with the lowest level of physical activity, the overall RR of ovarian cancer for the highest level of physical activity was 0.88 (95% confidence interval [CI] 0.75-1.03]. In subgroup meta-analyses by study design, there was no significant association in cohort studies (RR=1.09, 95% CI 0.84-1.41). However, a negative association was found in case-control studies (RR=0.73,95% CI 0.61-0.88). Conclusion: Current data provide limited support for the hypothesis that physical activity reduces the risk of ovarian cancer. More high-quality studies are required to confirm this finding. | |||
| TO cite this article:ZHAO Jitong,ZHOU Shengtao,LIN Xiaojuan. No Association Between Physical Activity and Risk of Ovarian Cancer: A Meta-analysis of Observational Studies[OL].[14 June 2016] http://en.paper.edu.cn/en_releasepaper/content/4697499 | |||
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