Small molecule activation of PKM2 in cancer cells induces serine auxotrophy.

نویسندگان

  • Charles Kung
  • Jeff Hixon
  • Sung Choe
  • Kevin Marks
  • Stefan Gross
  • Erin Murphy
  • Byron DeLaBarre
  • Giovanni Cianchetta
  • Shalini Sethumadhavan
  • Xiling Wang
  • Shunqi Yan
  • Yi Gao
  • Cheng Fang
  • Wentao Wei
  • Fan Jiang
  • Shaohui Wang
  • Kevin Qian
  • Jeff Saunders
  • Ed Driggers
  • Hin Koon Woo
  • Kaiko Kunii
  • Stuart Murray
  • Hua Yang
  • Katharine Yen
  • Wei Liu
  • Lewis C Cantley
  • Matthew G Vander Heiden
  • Shinsan M Su
  • Shengfang Jin
  • Francesco G Salituro
  • Lenny Dang
چکیده

Proliferating tumor cells use aerobic glycolysis to support their high metabolic demands. Paradoxically, increased glycolysis is often accompanied by expression of the lower activity PKM2 isoform, effectively constraining lower glycolysis. Here, we report the discovery of PKM2 activators with a unique allosteric binding mode. Characterization of how these compounds impact cancer cells revealed an unanticipated link between glucose and amino acid metabolism. PKM2 activation resulted in a metabolic rewiring of cancer cells manifested by a profound dependency on the nonessential amino acid serine for continued cell proliferation. Induction of serine auxotrophy by PKM2 activation was accompanied by reduced carbon flow into the serine biosynthetic pathway and increased expression of high affinity serine transporters. These data support the hypothesis that PKM2 expression confers metabolic flexibility to cancer cells that allows adaptation to nutrient stress.

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عنوان ژورنال:
  • Chemistry & biology

دوره 19 9  شماره 

صفحات  -

تاریخ انتشار 2012