What question did this study set out to answer?

To determine the regulatory mechanisms and functional impact of ENO2 acetylation on glycolysis and metastasis in pancreatic ductal adenocarcinoma.

May 12, 2020Signal Transduction and Targeted TherapyOpen Access

Insulin-like growth factor 1-induced enolase 2 deacetylation by HDAC3 promotes metastasis of pancreatic cancer

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Authors

YZYan Zheng CWChao Wu JYJimeng Yang

Discussion

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Overview

Preclinical study reveals that IGF-1 stimulates ENO2 deacetylation to fuel pancreatic cancer metastasis, suggesting IGF-1R inhibition as a therapeutic strategy.

Key Points

To determine the regulatory mechanisms and functional impact of ENO2 acetylation on glycolysis and metastasis in pancreatic ductal adenocarcinoma.
Assessed ENO2 expression across pancreatic ductal adenocarcinoma patient tissues and correlated levels with metastasis and patient survival.
Conducted knockdown and rescue experiments using wild-type and acetylation-mimetic (K394) ENO2 mutants to assess tumor growth and liver metastasis.
Investigated the signaling axis involving IGF-1, PI3K/AKT/mTOR, HDAC3 phosphorylation at S424, and pharmacological inhibition with linsitinib.
ENO2 was significantly overexpressed in PDAC tissues and correlated with tumor metastasis and decreased overall patient survival.
HDAC3 removed acetylation at the K394 site of ENO2, which activated its enzymatic function, accelerated glycolysis, and drove liver metastasis.
IGF-1 stimulated HDAC3 phosphorylation and ENO2 deacetylation via PI3K/AKT/mTOR signaling, an effect blocked by the IGF-1R inhibitor linsitinib.

Cite This Study

Zheng et al. (2020) studied this question.

synapsesocial.com/papers/6a86df78d75f6552a082aea1 https://doi.org/10.1038/s41392-020-0146-6

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May 12, 2020Signal Transduction and Targeted TherapyOpen Access

Insulin-like growth factor 1-induced enolase 2 deacetylation by HDAC3 promotes metastasis of pancreatic cancer

View Full Paper

Ask AI

Bookmark

Authors

YZYan Zheng CWChao Wu JYJimeng Yang

Discussion

Member takes

Overview

Preclinical study reveals that IGF-1 stimulates ENO2 deacetylation to fuel pancreatic cancer metastasis, suggesting IGF-1R inhibition as a therapeutic strategy.

Key Points

To determine the regulatory mechanisms and functional impact of ENO2 acetylation on glycolysis and metastasis in pancreatic ductal adenocarcinoma.
Assessed ENO2 expression across pancreatic ductal adenocarcinoma patient tissues and correlated levels with metastasis and patient survival.
Conducted knockdown and rescue experiments using wild-type and acetylation-mimetic (K394) ENO2 mutants to assess tumor growth and liver metastasis.
Investigated the signaling axis involving IGF-1, PI3K/AKT/mTOR, HDAC3 phosphorylation at S424, and pharmacological inhibition with linsitinib.
ENO2 was significantly overexpressed in PDAC tissues and correlated with tumor metastasis and decreased overall patient survival.
HDAC3 removed acetylation at the K394 site of ENO2, which activated its enzymatic function, accelerated glycolysis, and drove liver metastasis.
IGF-1 stimulated HDAC3 phosphorylation and ENO2 deacetylation via PI3K/AKT/mTOR signaling, an effect blocked by the IGF-1R inhibitor linsitinib.

Cite This Study

Zheng et al. (2020) studied this question.

synapsesocial.com/papers/6a86df78d75f6552a082aea1 https://doi.org/10.1038/s41392-020-0146-6

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