PKM2 phosphorylates MLC2 and regulates cytokinesis of tumour cells

Yuhui Jiang, Yugang Wang, Ting Wang, David H. Hawke, Yanhua Zheng, Xinjian Li, Qin Zhou, Sadhan Majumder, Erfei Bi, David X. Liu, Suyun Huang and Zhimin Lu ()
Additional contact information
Yuhui Jiang: The University of Texas MD Anderson Cancer Center
Yugang Wang: The University of Texas MD Anderson Cancer Center
Ting Wang: Perelman School of Medicine, University of Pennsylvania
David H. Hawke: The University of Texas MD Anderson Cancer Center
Yanhua Zheng: The University of Texas MD Anderson Cancer Center
Xinjian Li: The University of Texas MD Anderson Cancer Center
Qin Zhou: The M.O.E. Key Laboratory of Laboratory Medical Diagnostics, College of Laboratory Medicine, Chongqing Medical University
Sadhan Majumder: The University of Texas MD Anderson Cancer Center
Erfei Bi: Perelman School of Medicine, University of Pennsylvania
David X. Liu: Washington State University College of Pharmacy
Suyun Huang: The University of Texas MD Anderson Cancer Center
Zhimin Lu: The University of Texas MD Anderson Cancer Center

Nature Communications, 2014, vol. 5, issue 1, 1-14

Abstract: Abstract Pyruvate kinase M2 (PKM2) is expressed at high levels during embryonic development and tumour progression and is important for cell growth. However, it is not known whether it directly controls cell division. Here, we found that Aurora B phosphorylates PKM2, but not PKM1, at T45; this phosphorylation is required for PKM2’s localization and interaction with myosin light chain 2 (MLC2) in the contractile ring region of mitotic cells during cytokinesis. PKM2 phosphorylates MLC2 at Y118, which primes the binding of ROCK2 to MLC2 and subsequent ROCK2-dependent MLC2 S15 phosphorylation. PKM2-regulated MLC2 phosphorylation, which is greatly enhanced by EGF stimulation or EGFRvIII, K-Ras G12V and B-Raf V600E mutant expression, plays a pivotal role in cytokinesis, cell proliferation and brain tumour development. These findings underscore the instrumental function of PKM2 in oncogenic EGFR-, K-Ras- and B-Raf-regulated cytokinesis and tumorigenesis.

Date: 2014
References: Add references at CitEc
Citations: View citations in EconPapers (1)

Downloads: (external link)
https://www.nature.com/articles/ncomms6566 Abstract (text/html)

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:5:y:2014:i:1:d:10.1038_ncomms6566

Ordering information: This journal article can be ordered from
https://www.nature.com/ncomms/

DOI: 10.1038/ncomms6566

Access Statistics for this article

Nature Communications is currently edited by Nathalie Le Bot, Enda Bergin and Fiona Gillespie

More articles in Nature Communications from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().