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Fang-Ming Chen,Hsueh-Wei Chang,Sheau-Fang Yang,Ya-Fang Huang,Pei-Yung Nien,Yao-Tsung Yeh,Ming-Feng Hou 생화학분자생물학회 2012 Experimental and molecular medicine Vol.44 No.5
The mitogen-activated protein kinase (MAPK) phosphatase-1 (MKP-1) belongs to the MAPK cascades which are central to cell proliferation and apoptosis. The carcinogenic role of MKP-1 has been reported in many types of cancer but it has rarely been investigated in breast cancer. The present study was designed to evaluate the MKP-1 mRNA expression and its possible regulation by methylation of MKP-1 promoter in the model of several breast cancer cell lines and tissues as well as controls. Our data demonstrate MKP-1mRNA expression significantly decreased in five breast cancer cell lines compared to breast controls (P <0.01). Using the methylation-specific PCR (MSP) analysis,the unmethylated reaction (U) is dominant in both normal cell lines and benign breast tumors (100% vs. 86.2%), whereas the methylated reaction (M) is dominant in both breast cancer cell lines and invasive breast tumors (100% vs. 57.2%). In terms of methylation ratio (M/M+U), methylation level in MKP-1 promoter is significantly higher in the invasive breast tumor tissues (n = 152) than in benign breast tumor tissues (n = 29)(P < 0.0001). Assessing the methylation ratio of the promoter of MKP-1 gene to diagnose the breast malignancy (invasive vs. benign), the area under the receiver-operating characteristic (ROC) curve was 0.809(95% CI: 0.711-0.906, P < 0.001). The best performance for this prediction has a sensitivity of 76.32% and a specificity of 82.76% at the cutoff value of 0.38. Taken together, we firstly demonstrated that the promoter methylation of MKP-1 gene is a potential breast cancer biomarker for breast malignancy.
Application of BIM on Drawing Verification of Firefighting
Chang, Ya-Chun,Shr, Jin-Fang,Huang, Xuan-Chao The Society for Aerospace System Engineering 2015 International Journal of Aerospace System Engineer Vol.2 No.2
In general, most of the function and using of building is for single purpose. However, current buildings combine several functions that causes a lot of problems not on firefighting only but also on environment engineering. Because of hard integration on different fields that causes a lot of conflict. That wastes cost and time. That also threaten the safety of firefighting. This search focuses on the drawing verification and field inspection on firefighting. These two items both remain paper work. To complete the current work, it needs to bring a great amount of drawing papers in the field. By BIM, integrated data can be extracted. It makes the drawing verification and field inspection easier and increases the efficiency. That is the main point of this research.
Sulforaphane Inhibits the Proliferation of the BIU87 Bladder Cancer Cell Line via IGFBP-3 Elevation
Dang, Ya-Mei,Huang, Gang,Chen, Yi-Rong,Dang, Zhong-Feng,Chen, Cheng,Liu, Feng-Lei,Guo, Ying-Fang,Xie, Xiao-Dong Asian Pacific Journal of Cancer Prevention 2014 Asian Pacific journal of cancer prevention Vol.15 No.4
Aim: To investigate effects of sulforaphane on the BIU87 cell line and underlying mechanisms involving IGFBP-3. Methods: Both BIU87 and IGFBP-3-silenced BIU87 cells were treated with sulforaphane. Cell proliferation was detected by MTT assay. Cell cycle and apoptosis were determined via flow cytometry. Quantitative polymerase chain reaction and Western blotting were applied to analyze the expression of IGFBP-3 and NF-${\kappa}B$ at both mRNA and protein levels. Results: Sulforaphane (80 ${\mu}M$) treatment could inhibit cell proliferation, inducing apoptosis and cell cycle arrest at G2/M phase. All these effects could be antagonized by IGFBP-3 silencing. Furthermore, sulforaphane (80 ${\mu}M$) could down-regulate NF-${\kappa}B$ expression while elevating that of IGFBP-3. Conclusions: Sulforaphane could suppress the proliferation of BIU87 cells via enhancing IGFBP-3 expression, which negatively regulating the NF-${\kappa}B$ signaling pathway.
Ets-1 enhances tumor migration through regulation of CCR7 expression
( Li-wen Fang ),( Ying-hsien Kao ),( Ya-ting Chuang ),( Huey-lan Huang ),( Tzong-shyuan Tai ) 생화학분자생물학회(구 한국생화학분자생물학회) 2019 BMB Reports Vol.52 No.9
Ets-1 is a prototype of the ETS protein family. Members of the ETS protein family contain a unique ETS domain. Ets-1 is associated with cancer progression and metastasis in many types of cancer. Many studies have shown a link between elevated expression of Ets-1 in cancer biopsies and poor survival. CCR7 is a chemokine that binds to specific ligand CCL21/CCL19. CCR7 expression is associated with tumor metastasis and infiltration into lymph nodes. The objective of this study was to test whether Ets-1 could regulate CCR7 expression and enhance tumor metastasis. Our data showed that CCR7 expression was downregulated in Ets-1-deficient T cells upon T-cell stimulation. Overexpression of Ets-1 increased CCR7 expression in breast cancer cell lines. In contrast, knockdown of Ets-1 reduced CCR7 expression. Ets-1 could directly bind to CCR7 promoter and mediate CCR7 expression in luciferase reporter assays and chromatin immunoprecipitation assays. Transactivation activity of Ets-1 was independent of the Pointed domain of Ets-1. Ets-1 could also enhance NF- κB and CBP transactivation of CCR7 promoter. Our results also showed that Ets-1 could modulate cancer cell transmigration by altering CCR7 expression in transwell assay and wound healing assay. Taken together, our data suggest that Ets-1 can enhance CCR7 expression and contribute to tumor cell migration. [BMB Reports 2019; 52(9): 548-553]
ALGORITHMS FOR SYSTEMS OFNONLINEAR VARIATIONAL INEQUALITIES
Yeol Je Cho,Ya-ping Fang,Nan-jing Huang,Ho Jin Hwang 대한수학회 2004 대한수학회지 Vol.41 No.3
In this paper, we introduce and study a new system of nonlinear variational inequalities. The existence and uniqueness of solution for this problem are proved and an iterative algorithm for approximating the solution of system of nonlinear variational inequalities is constructed.
Patient and Care Delays of Breast Cancer in China
Yue-Lin Li,Ya-Chao Qin,Lu-Ying Tang,Yu-Huang Liao,Wei Zhang,Xiao-Ming Xie,Qiang Liu,Ying Lin,Ze-Fang Ren 대한암학회 2019 Cancer Research and Treatment Vol.51 No.3
Purpose This study differentiates patient and care delays of breast cancer and explores the related factors as well as the associations with the prognosis in Guangzhou, a southern city of China. Materials and Methods A cohort of female incident breast cancer patients (n=1,551) was recruited from October 2008 to March 2012 and followed up until January 1, 2016 (n=1,374) in the affiliated hospitals of Sun Yat-sen University. The factors associated with patient and care delays were analyzed with multivariable logistic models. Cox proportional hazards regression models were constructed to estimate the impacts of the delays on the prognosis. Results There were 40.4% patient delay (! 3 months) and 15.5% care delay (! 1 month). The patient delay, but not the care delay, was significantly related to the clinical stage and consequently worsened the prognosis of breast cancer (hazard ratio, 1.45; 95% confidence interval, 1.09 to 1.91 for progression-free survival). The factors related to an increased patient delay included premenopausal status, history of benign breast disease, and less physical examination. Conclusion Patient delay was the main type of delay in Guangzhou and resulted in higher clinical stage and poor prognosis of breast cancer. Screening for breast cancer among premenopausal women may be an effective way to reduce this delay.