Searching the Resource Information Network

Our searching services are busy right now. Please try again later

  • Register
X
Forgot Password

If you have forgotten your password you can enter your email here and get a temporary password sent to your email.

X

Leaving Community

Are you sure you want to leave this community? Leaving the community will revoke any permissions you have been granted in this community.

No
Yes

O-GlcNAcase targets pyruvate kinase M2 to regulate tumor growth.

Jay Prakash Singh | Kevin Qian | Jeong-Sang Lee | Jinfeng Zhou | Xuemei Han | Bichen Zhang | Qunxiang Ong | Weiming Ni | Mingzuo Jiang | Hai-Bin Ruan | Min-Dian Li | Kaisi Zhang | Zhaobing Ding | Philip Lee | Kamini Singh | Jing Wu | Raimund I Herzog | Susan Kaech | Hans-Guido Wendel | John R Yates | Weiping Han | Robert S Sherwin | Yongzhan Nie | Xiaoyong Yang
Oncogene | 2020

Cancer cells are known to adopt aerobic glycolysis in order to fuel tumor growth, but the molecular basis of this metabolic shift remains largely undefined. O-GlcNAcase (OGA) is an enzyme harboring O-linked β-N-acetylglucosamine (O-GlcNAc) hydrolase and cryptic lysine acetyltransferase activities. Here, we report that OGA is upregulated in a wide range of human cancers and drives aerobic glycolysis and tumor growth by inhibiting pyruvate kinase M2 (PKM2). PKM2 is dynamically O-GlcNAcylated in response to changes in glucose availability. Under high glucose conditions, PKM2 is a target of OGA-associated acetyltransferase activity, which facilitates O-GlcNAcylation of PKM2 by O-GlcNAc transferase (OGT). O-GlcNAcylation inhibits PKM2 catalytic activity and thereby promotes aerobic glycolysis and tumor growth. These studies define a causative role for OGA in tumor progression and reveal PKM2 O-GlcNAcylation as a metabolic rheostat that mediates exquisite control of aerobic glycolysis.

Pubmed ID: 31501520

Research resources used in this publication

None found

Antibodies used in this publication

None found

Associated grants

  • Agency: NIDDK NIH HHS, United States
    Id: P01 DK057751
  • Agency: NCI NIH HHS, United States
    Id: P30 CA008748
  • Agency: NIDDK NIH HHS, United States
    Id: R01 DK089098

Publication data is provided by the National Library of Medicine ® and PubMed ®. Data is retrieved from PubMed ® on a weekly schedule. For terms and conditions see the National Library of Medicine Terms and Conditions.

This is a list of tools and resources that we have found mentioned in this publication.


PeproTech (tool)

RRID:SCR_006802

An Antibody supplier

View all literature mentions

Adobe Photoshop (tool)

RRID:SCR_014199

Software for image processing, analysis, and editing. The software includes features such as touch capabilities, a customizable toolbar, 2D and 3D image merging, and Cloud access and options.

View all literature mentions

NCI-H1299 (tool)

RRID:CVCL_0060

Cell line NCI-H1299 is a Cancer cell line with a species of origin Homo sapiens (Human)

View all literature mentions

MCF-10A (tool)

RRID:CVCL_0598

Cell line MCF-10A is a Spontaneously immortalized cell line with a species of origin Homo sapiens

View all literature mentions

HeLa (tool)

RRID:CVCL_0030

Cell line HeLa is a Cancer cell line with a species of origin Homo sapiens

View all literature mentions

MCF-7 (tool)

RRID:CVCL_0031

Cell line MCF-7 is a Cancer cell line with a species of origin Homo sapiens (Human)

View all literature mentions

HEK293T (tool)

RRID:CVCL_0063

Cell line HEK293T is a Transformed cell line with a species of origin Homo sapiens (Human)

View all literature mentions

A-549 (tool)

RRID:CVCL_0023

Cell line A-549 is a Cancer cell line with a species of origin Homo sapiens (Human)

View all literature mentions