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Abstract B22: Loss of LncRNA XIST induces Epithelial to Mesenchymal Transition in Breast Cancer
Brain is one of the major sites of metastasis of breast cancer, and approximately 20% of patients with aggressive breast cancer eventually develop the metastatic disease in the brain. Long non-coding RNAs (lncRNA) have recently drawn much attention due to their wide functional variations and potential roles in tumor progression. By performing lncRNA array analysis comparing non-metastatic primary tumors with brain metastatic tumors from breast cancer patients, we identified that lncRNA XIST expression was significantly down-regulated in brain metastatic tumors. The result of Taqman PCR validated the results in tumor sample...
Source: Cancer Research - May 25, 2016 Category: Cancer & Oncology Authors: Liu, Y., Xing, F., Wu, K., Sharma, S., Watabe, K. Tags: Genetics and Evolution of Metastatic Tumors Source Type: research

Abstract A07: Knockdown laminin-511 expression blocked endlthelial cell function in vitro and angiogenesis in vivo knockout skin model
In conclusion, our data suggested a possible involvement of laminin-511 in integrin alphaV and beta3-dependent angiogenesis and blood vessel maturation. Our works revealed the important roles of laminin-511 in endothelial cell activities, which proved its significance for angiogenesis.Citation Format: Jie Li, Tengjiao Cui. Knockdown laminin-511 expression blocked endlthelial cell function in vitro and angiogenesis in vivo knockout skin model. [abstract]. In: Proceedings of the AACR Special Conference: Tumor Angiogenesis and Vascular Normalization: Bench to Bedside to Biomarkers; Mar 5-8, 2015; Orlando, FL. Philadelphia (PA...
Source: Molecular Cancer Therapeutics - December 6, 2015 Category: Cancer & Oncology Authors: Li, J., Cui, T. Tags: Antiangiogenic Therapy: Poster Presentations - Proffered Abstracts Source Type: research

Abstract A13: Mechanisms of E47 induced quiescence and acinar cell differentiation in human pancreatic cancer cells
Pancreatic ductal adenocarcinoma (PDA) initiates from quiescent acinar cells that attain a Kras mutation, undergo acinar-ductal metaplasia and rapidly acquire increased growth potential. During this process several transcription factors from the basic helix-loop-helix (bHLH) family are downregulated while expression of their inhibitor Id3 is induced. Previously we showed that Id3 knockdown with siRNA resulted in growth arrest in PDA cells. Here we queried whether aggressive PDA cells can be reprogrammed to revert to their original quiescent acinar cell phenotype by shifting bHLH transcription programs. In order to mitigate...
Source: Cancer Research - June 30, 2015 Category: Cancer & Oncology Authors: Kim, S., Yang, C., Riha, C., Lamy, R., Jakubison, B. L., Konieczny, S. F., Itkin-Ansari, P. Tags: Development Source Type: research