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Articles by W Liang
Total Records ( 3 ) for W Liang
  P Wang , Z Chen , Z. Q Meng , J Fan , J. M Luo , W Liang , J. H Lin , Z. H Zhou , H Chen , K Wang , Y. H Shen , Z. D Xu and L. M. Liu

Ski used to be defined as an oncogene that contributes to the resistance of tumor cells to transforming growth factor-β (TGF-β)-induced growth arrest. As TGF-β has a dual effect on tumor growth with both tumor-suppressing and -promoting activity depending on the stage of carcinogenesis and the cell type, the precise role of Ski in carcinogenesis remains unclear. In this study, we show that downregulation of Ski through lentivirus-mediated RNA interference decreases tumor growth both in vitro and in vivo, yet promotes cell invasiveness in vitro, and lung metastasis in vivo in the pancreatic cancer cell line SW1990, which contain wild-type Smad4 expression, and the BxPC3 cell line, which is Smad4 deficient. We also show that the downregulation of Ski increases TGF-β-induced transcriptional activity, which is associated with increased TGF-β-dependent Smad2/3 phosphorylation, and results in an altered expression profile of TGF-β-inducible genes involved in metastasis, angiogenesis and cell proliferation and epithelial–mesenchymal transition. Immunohistochemical analysis of specimens from 71 patients with pancreatic adenocarcinoma showed a significant association between overexpression of Ski and decreased patient survival time (P = 0.0024). Our results suggest that Ski may act as a tumor proliferation-promoting factor or as a metastatic suppressor in human pancreatic cancer.

  D Guo , Z Kassiri , R Basu , F. L Chow , V Kandalam , F Damilano , W Liang , S Izumo , E Hirsch , J. M Penninger , P. H Backx and G. Y. Oudit

Mechanotransduction and the response to biomechanical stress is a fundamental response in heart disease. Loss of phosphoinositide 3-kinase (PI3K), the isoform linked to G protein–coupled receptor signaling, results in increased myocardial contractility, but the response to pressure overload is controversial.


To characterize molecular and cellular responses of the PI3K knockout (KO) mice to biomechanical stress.

Methods and Results:

In response to pressure overload, PI3KKO mice deteriorated at an accelerated rate compared with wild-type mice despite increased basal myocardial contractility. These functional responses were associated with compromised phosphorylation of Akt and GSK-3. In contrast, isolated single cardiomyocytes from banded PI3KKO mice maintained their hypercontractility, suggesting compromised interaction with the extracellular matrix as the primary defect in the banded PI3KKO mice. β-Adrenergic stimulation increased cAMP levels with increased phosphorylation of CREB, leading to increased expression of cAMP-responsive matrix metalloproteinases (MMPs), MMP2, MT1-MMP, and MMP13 in cardiomyocytes and cardiofibroblasts. Loss of PI3K resulted in increased cAMP levels with increased expression of MMP2, MT1-MMP, and MMP13 and increased MMP2 activation and collagenase activity in response to biomechanical stress. Selective loss of N-cadherin from the adhesion complexes in the PI3KKO mice resulted in reduced cell adhesion. The β-blocker propranolol prevented the upregulation of MMPs, whereas MMP inhibition prevented the adverse remodeling with both therapies, preventing the functional deterioration in banded PI3KKO mice. In banded wild-type mice, long-term propranolol prevented the adverse remodeling and systolic dysfunction with preservation of the N-cadherin levels.


The enhanced propensity to develop heart failure in the PI3KKO mice is attributable to a cAMP-dependent upregulation of MMP expression and activity and disorganization of the N-cadherin/β-catenin cell adhesion complex. β-Blocker therapy prevents these changes thereby providing a novel mechanism of action for these drugs.

  M Zheng , W Liang , H Yu and Y. Xiao

In the following paper, we study the tradeoff between network utility and network lifetime for energy-constrained wireless sensor networks (WSNs). By introducing a weighted factor, we combine these two objectives into a single weighted objective, and we consider rate control and routing in this tradeoff framework simultaneously. First, by using a dual decomposition method, we decompose the tradeoff model into two subproblems: the congestion control/routing problem and the network lifetime problem, both of which interact through the dual variables for energy dissipation constraints. Based on the decomposition results, we propose a fully distributed algorithm to solve these two sub-problems and the dual problem by using gradient and sub-gradient projection methods. Second, we propose a fully distributed algorithm by approximating the network lifetime maximization problem by using the network utility maximization (NUM) framework. Third, we extend our distributed algorithm to deal with reliable communication and the real-time requirement. Rigorous analysis and simulations are presented to validate our algorithms.

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