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An Integrated Transcriptomics and Proteomics Analysis Implicates lncRNA MALAT1 in the Regulation of Lipid Metabolism.

Abstract
Long noncoding RNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is upregulated in various cancers, and its overexpression is associated with tumor growth and metastasis. MALAT1 has been recognized as a key player in the regulation of RNA splicing and transcription; however, the landscape of gene expression regulated by MALAT1 remains unclear. In this study, we employed an integrated transcriptomics and proteomics strategy to characterize the alterations in gene expression induced by MALAT1 knockdown in hepatocellular carcinoma (HCC) cells and identified 2662 differentially expressed transcripts and 1149 differentially expressed proteins. Interestingly, downregulation of MALAT1 reduced the abundances of multiple genes in the AMP-activated protein kinase (AMPK) signaling and biosynthesis of unsaturated fatty acids pathways. Further investigation showed that MALAT1 knockdown inhibited glucose uptake and lipogenesis by reducing the expression levels of these lipid metabolism related genes, which contributes to the oncogenic role of MALAT1 in tumor cell proliferation and invasion. This study uncovers the function of MALAT1 in the modulation of cancer lipid metabolism, reveals the underlying molecular mechanism, and further supports the potential therapeutic opportunities for targeting MALAT1 in HCC treatment.
AuthorsHao Wang, Yali Zhang, Xinyu Guan, Xing Li, Zhenwen Zhao, Yan Gao, Xiangyang Zhang, Ruibing Chen
JournalMolecular & cellular proteomics : MCP (Mol Cell Proteomics) Vol. 20 Pg. 100141 ( 2021) ISSN: 1535-9484 [Electronic] United States
PMID34478876 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
CopyrightCopyright © 2021 The Authors. Published by Elsevier Inc. All rights reserved.
Chemical References
  • MALAT1 long non-coding RNA, human
  • RNA, Long Noncoding
Topics
  • Carcinoma, Hepatocellular (genetics, metabolism, pathology)
  • Cell Line
  • Cell Movement
  • Cell Proliferation
  • Gene Expression Regulation, Neoplastic
  • Humans
  • Lipid Metabolism (genetics)
  • Liver (metabolism)
  • Liver Neoplasms (genetics, metabolism, pathology)
  • Proteomics
  • RNA, Long Noncoding
  • Transcriptome
  • Wound Healing

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