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.

Alert Name:
Alerting to:
Authentication email will be sent to your email address in 24 hours
Frequency:
Email Message Format:	Plain text Graphical(HTML)

Complete the form below and we will recommend the selected titles to your friends on your behalf. * Indicates a required field.
Your name*:
Your email address*:
Recipient's name*:
Recipient's email address*:
(multiple recipient's names and email addresses should be separated with semicolons)
Your comments:	I thought you would find the page(s) useful.

Your name:
Your email address:
Recipient's name:
Recipient's email address:
(multiple recipient's names and email addresses should be separated with semicolons)
Your comments:	I thought you would find this page useful.

Disclaimer: This message was sent to your friend using the "Send it to a friend" facility on the Sciencepaper Online’ WWW site, http://www.paper.edu.cn/en. The Sciencepaper Online is not responsible for the content of this email, and anything said in this email does not necessarily reflect the Sciencepaper Online's views.


	1. 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
	Show/Hide Abstract \| Cite this paper︱Full-text: PDF (456K B)

	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


	2. 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
	Show/Hide Abstract \| Cite this paper︱Full-text: PDF (882K B)

	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

Saved Papers

Saved Papers


	3. 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
	Show/Hide Abstract \| Cite this paper︱Full-text: PDF (4K B)

	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


	4. 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
	Show/Hide Abstract \| Cite this paper︱Full-text: PDF (4K B)

	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


	5. 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
	Show/Hide Abstract \| Cite this paper︱Full-text: PDF (4K B)

	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


	6. 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
	Show/Hide Abstract \| Cite this paper︱Full-text: PDF (4K B)

	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


	7. 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
	Show/Hide Abstract \| Cite this paper︱Full-text: PDF (4K B)

	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


	8. 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
	Show/Hide Abstract \| Cite this paper︱Full-text: PDF (4K B)

	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


	9. LAPTM4B Expression Predicts Chemoresistance and Poor Clinical Outcomes in Patients with Local Advanced Cervical Cancer Treated with Neoadjuvant Chemotherapy Prior to Radical Hysterectomy
	Fanling Meng,Pan shang,Hongtao Song,Ge Lou
	Clinical Medicine 07 June 2016
	Show/Hide Abstract \| Cite this paper︱Full-text: PDF (4K B)

	Abstract:Objectives: LAPTM4B (lysosomal protein transmembrane-4 beta) plays a critical role in tumor progression and chemoresistance. The aim of this study was to evaluate the significance of LAPTM4B expression to predict response to platinum-based neoadjuvant chemotherapy and survival of patients with locally advanced cervical cancer (LACC) who subsequently underwent radical hysterectomy. Materials and methods: Biopsy specimens of cervical cancer before neoadjuvant chemotherapy were obtained from 116 patients who subsequently underwent radical hysterectomy. The expression of LAPTM4B protein was analyzed by immunohistochemistry. Findings were evaluated in relation to LAPTM4B expression and chemotherapy resistance. Survival analyses were performed by the Kaplan-Meier curves and a Cox regression model to determine overall survival (OS) and disease-free survival (DFS). Results: Our result showed that LAPTM4B was highly expressed in 73.3% of LACC sections. Expression of LAPTM4B was significantly associated with poor clinical response (P=0.012). Moreover, high expression of LAPTM4B was significantly associated with poor OS and DFS compared with the low expression group (both P<0.05). Multivariate analysis revealed that LAPTM4B expression was an independent prognostic factor for OS (P<0.05). Conclusions: In conclusion, elevated LAPTM4B expression in patients with locally advanced cervical cancer contributes to chemoresistance and predicts poor prognosis.
	TO cite this article:Fanling Meng,Pan shang,Hongtao Song, et al. LAPTM4B Expression Predicts Chemoresistance and Poor Clinical Outcomes in Patients with Local Advanced Cervical Cancer Treated with Neoadjuvant Chemotherapy Prior to Radical Hysterectomy[OL].[ 7 June 2016] http://en.paper.edu.cn/en_releasepaper/content/4693514


	10. Over-expression of LAPTM4B-35 and VEGF is related to poor prognosis in local advanced cervical carcinoma
	Fanling Meng,Pan Shang,Hongtao Song,Ge Lou
	Clinical Medicine 04 June 2016
	Show/Hide Abstract \| Cite this paper︱Full-text: PDF (4K B)

	Abstract:Objectives: Patients with locally advanced cervical cancer (LACC) are difficult to treat. The purpose of this study is to investigate lysosome-associated protein transmembrane 4?-35 (LAPTM4B-35) and vascular endothelial growth factor (VEGF) expression in LACC and evaluate their clinicopathological and prognostic significance. Methods: The expression of LAPTM4B-35 and VEGF proteins was analyzed by immunohistochemistry in 119 LACC and 40 normal cervical specimens. Results: LAPTM4B-35 and VEGF were expressed in 73.9% and 75.6% of cervical cancer, respectively, which are higher than the normal cervical tissues. LAPTM4B-35 expression was positively correlated with the expression of VEGF. The expression of LAPTM4B-35 and VEGF was significantly correlated with FIGO stage, Histological grade and lymph node metastasis (P<0.05). Kaplan-Meier analysis showed that LACC patients with high expression of LAPTM4B-35 and VEGF exhibited poor overall survival (OS) and disease-free survival (DFS) (P<0.05). Conclusions: We demonstrate that LAPTM4B-35 correlates with VEGF and is a poor prognostic factor in local advanced cervical cancer.
	TO cite this article:Fanling Meng,Pan Shang,Hongtao Song, et al. Over-expression of LAPTM4B-35 and VEGF is related to poor prognosis in local advanced cervical carcinoma[OL].[ 4 June 2016] http://en.paper.edu.cn/en_releasepaper/content/4693517

	Check out RSS, or use RSS reader to subscribe this item