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Pyruvate kinase L/R is a regulator of lipid metabolism and mitochondrial function

Artikel i vetenskaplig tidskrift
Författare Z. T. Liu
C. Zhang
S. Lee
W. Kim
Martina Klevstig
A. M. Harzandi
N. Sikanic
M. Arif
Marcus Ståhlman
J. Nielsen
M. Uhlen
Jan Borén
A. Mardinoglu
Publicerad i Metabolic Engineering
Volym 52
Sidor 263-272
ISSN 1096-7176
Publiceringsår 2019
Publicerad vid Institutionen för medicin, avdelningen för molekylär och klinisk medicin
Sidor 263-272
Språk en
Länkar dx.doi.org/10.1016/j.ymben.2019.01....
Ämnesord fatty liver-disease, analysis reveals, DNA-replication, database, association, stress, models, tools, risk, Biotechnology & Applied Microbiology
Ämneskategorier Klinisk medicin

Sammanfattning

The pathogenesis of non-alcoholic fatty liver disease (NAFLD) and hepatocellular carcinoma (HCC) has been associated with altered expression of liver-specific genes including pyruvate kinase liver and red blood cell (PKLR), patatin-like phospholipase domain containing 3 (PNPLA3) and proprotein convertase subtilisin/kexin type 9 (PCSK9). Here, we inhibited and overexpressed the expression of these three genes in HepG2 cells, generated RNA-seq data before and after perturbation and revealed the altered global biological functions with the modulation of these genes using integrated network (IN) analysis. We found that modulation of these genes effects the total triglycerides levels within the cells and viability of the cells. Next, we generated IN for HepG2 cells, identified reporter transcription factors based on IN and found that the modulation of these genes affects key metabolic pathways associated with lipid metabolism (steroid biosynthesis, PPAR signalling pathway, fatty acid synthesis and oxidation) and cancer development (DNA replication, cell cycle and p53 signalling) involved in the progression of NAFLD and HCC. Finally, we observed that inhibition of PKLR lead to decreased glucose uptake and decreased mitochondrial activity in HepG2 cells. Hence, our systems level analysis indicated that PKLR can be targeted for development efficient treatment strategy for NAFLD and HCC.

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