NDLI: CIP2A regulates cancer metabolism and CREB phosphorylation in non-small cell lung cancer.

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Year: 2014 Volume: 10

CIP2A regulates cancer metabolism and CREB phosphorylation in non-small cell lung cancer.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Peng, Bo Lei, Ningjing Chai, Yurong Chan, Edward K. L. Zhang, Jian-Ying
Description	Country affiliation: United States Author Affiliation: Peng B ( Border Biomedical Research Center & Department of Biological Sciences, The University of Texas at El Paso, El Paso, Texas 79968, USA. jzhang@utep.edu.)
Abstract	The cancerous inhibitor of protein phosphatase 2A (CIP2A) is a recently characterized endogenous inhibitor of the phosphatase activity of protein phosphatase 2A (PP2A), which extends the half-life of oncogenic protein c-myc and promotes in vivo tumor growth. The function of CIP2A in cancer progression is still poorly understood. To uncover the underlying mechanism of CIP2A-mediated cell proliferation, we implemented a two-dimensional electrophoresis (2DE)-based proteomic approach to examine lung cancer cell H1299 with and without CIP2A. We found 47 proteins differentially expressed where 19 proteins were upregulated and 28 proteins were downregulated. These were categorized into functional groups such as metabolism (25%), transcriptional and translational control (23%), and the signaling pathway and protein degradation (20%). On one hand, we validate our proteomic work by measuring the metabolic change. The knockdown of CIP2A decreased the expression of LDH-A as well as the enzymatic activity, accompanying with a decreased lactate production, an increased NADH/NAD+ ratio and ROS production. On the other hand, we found that CIP2A may regulate CREB activity through bioinformatics analysis. Our following experiments showed that, CIP2A positively regulated the phosphorylation of CREB in response to the serum treatment. Therefore, our proteomic study suggested that CIP2A mediates cancer progression through the metabolic pathway and intracellular signaling cascade.
File Format	HTM / HTML
ISSN	1742206X
e-ISSN	17422051
DOI	10.1039/c4mb00513a
Journal	Molecular BioSystems
Issue Number	1
Volume Number	11
Language	English
Publisher	Royal Society of Chemistry
Publisher Date	2015-01-01
Publisher Place	Great Britain (UK)
Access Restriction	Open
Subject Keyword	Discipline Molecular Biology Discipline Biochemistry Autoantigens Metabolism Carcinoma, Non-small-cell Lung Cyclic Amp Response Element-binding Protein Energy Metabolism Lung Neoplasms Membrane Proteins Genetics Cell Line, Tumor Cell Proliferation Gene Expression Gene Expression Regulation, Neoplastic Gene Knockdown Techniques Isoenzymes L-lactate Dehydrogenase Protein Interaction Maps Proteome Proteomics Rna, Small Interfering Reactive Oxygen Species Signal Transduction Transcription, Genetic Transfection Tumor Stem Cell Assay Research Support, N.i.h., Extramural
Content Type	Text
Resource Type	Article
Subject	Molecular Biology Biotechnology

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