Pkm2 can enhance pluripotency in ESCs and promote somatic cell reprogramming to iPSCs

// Shengtang Qin 1, * , Danli Yang 1, * , Kang Chen 1, * , Haolan Li 1 , Liqiang Zhang 1 , Yuan Li 1 , Rongrong Le 2 , Xiaojie Li 3 , Shaorong Gao 2 and Lan Kang 1 1 Institute of Cancer Stem Cell, Dalian Medical University, Dalian 116044, China 2 School of Life Sciences and Technology, Tongji University, Shanghai 200092, China 3 College of Stomatology, Dalian Medical University, Dalian 116044, China * These authors have contributed equally to this work Correspondence to: Lan Kang, email: kanglan@dlmedu.edu.cn Shaorong Gao, email: gaoshaorong@tongji.edu.cn Xiaojie Li, email: xiaojieli0504@dlmedu.edu.cn Keywords: Pkm2, ESC, iPSC, reprogramming, pluripotency Received: April 27, 2017      Accepted: July 25, 2017      Published: September 06, 2017 ABSTRACT Aerobic glycolysis is one of the most important common characteristics in both cancer cells and stem cells. Metabolism switch has been discovered as an important early event in the process of reprogramming somatic cells to induced pluripotent stem cells (iPSCs). As a rate limiting kinase in glycolysis, Pkm2 has been reported playing critical roles in many tumors, yet its role in stem cells and iPSCs induction is poorly defined. In the present study, we showed that Pkm2 is a predominant pyruvate kinase in embryonic stem cells (ESCs), and its expression increases many pluripotent genes. During somatic cell reprogramming, up-regulation of Pkm2 can be observed and over-expression of Pkm2 can facilitate iPSCs induction, while Pkm1 or a mutant form of Pkm2 (Pkm2 K422R ) showed no enhancement role in iPSCs induction. Therefore, our data demonstrated that Pkm2 enhances the pluripotency maintenance in ESCs and promotes the pluripotency acquisition during somatic cell reprogramming.