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Mutant Kras drives pancreatic cancer maintenance via metabolic pathways
Date:4/26/2012

supports production of building blocks for cancer growth

Transcriptome analysis of gene activation in the iKras/p53 null tumors after Kras extinction indicated decreased activity of genes involved in metabolism.

Metabolic studies showed that Kras extinction led to decreases in intermediates involved in glucose metabolism and reduced glucose uptake and lactate production. The metabolic changes correlated with the gene expression changes identified by transcription analysis.

The affected glucose intermediates are used in other glucose-utilizing pathways, which led the team to analyze the hexosamine biosynthesis pathway (HBP) and the pentose phosphate pathway, both of which are involved in the construction of cellular building blocks, including assembly of DNA and RNA.

They found that with Kras extinct, protein glycosylation via the HBP, an important signaling step in many cellular processes, is reduced to levels that are observed under conditions of glucose starvation.

The pentose phosphate pathway (PPP) uses glucose to generate ribose rings, an essential component of DNA and RNA, and to maintain the cell's ability to store electrons in NADPH. This pathway has two arms, a well-characterized oxidative arm and a less well-understood nonoxidative arm.

Kras extinction had no effect on glucose flux through the oxidative arm but led to decreases in glucose levels in components of the nonoxidative arm involved in ribose synthesis. Radioactive labeling of C-glucose showed a dramatic drop in labeled glucose incorporated into DNA/RNA when Kras is extinct.

Expression levels of enzymes involved in the nonoxidative PPP arm also fell under Kras extinction. Knockdown of either Rpia, Rpe or both enzymes reduced glucose flux into DNA/RNA and also suppressed tumor growth.

Inhibiting MAPK, Myc is similar to Kras extinction

The team then inhibited separate components of the Kras pathway to identify
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Contact: Scott Merville
smerville@mdanderson.org
713-792-0661
University of Texas M. D. Anderson Cancer Center
Source:Eurekalert

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