Loss of FBP1 by Snail-mediated Repression Provides Metabolic Advantages in Basal-like Breast Cancer

By Chenfang Dong, Tingting Yuan, Yadi Wu, Yifan Wang, T. Fan, Sumitra Miriyala, Yiwei Lin, Jun Yao, Jian-Ting Shi, Tiebang Kang and 5 more. Cancer Cell, 2013

733 citations recorded by the source corpus.

SUMMARY Epithelial-mesenchymal transition (EMT) enhances invasiveness and confers tumor cells with cancer stem cell (CSC)-like characteristics. We showed that the Snail-G9a-Dnmt1 complex, which is critical for E-cadherin promoter silencing, is also required for the promoter methylation of fructose-1,6-biphosphatase (FBP1) in basal-like breast cancer (BLBC). Loss of FBP1 induces glycolysis and results in increased glucose uptake, macromolecules biosynthesis, formation of tetrameric PKM2, and maintenance of ATP production under hypoxia. Loss of FBP1 also inhibits oxygen consumption and ROS production by suppressing mitochondrial complex I activity; this metabolic reprogramming results in an increased CSC-like property and tumorigenicity by enhancing the interaction of β-catenin with TCF. Our study indicates that the loss of FBP1 is a critical oncogenic event in EMT and BLBC.

Subfields: Cancer Research, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/d0b3e770b9dc1961b6f977cf5c2d34bbf60fe36f

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cancer Research

1. Ming Tan
2. Qingsong Cai
3. Jianrong Lu

In Molecular Biology

1. Ming Tan
2. Binhua P. Zhou
3. Qingsong Cai
4. Jianrong Lu

In Oncology

1. Ming Tan
2. Binhua P. Zhou
3. Qingsong Cai
4. Jianrong Lu

Citations in the corpus

• The Warburg effect in tumor progression: Mitochondrial oxidative metabolism as an anti-metastasis mechanism (2014, background): “Increased Snail expression inhibits COX expression and activity, and consequently represses oxygen consumption and mitochondrial respiration [73].”
• The Role of Snail in EMT and Tumorigenesis (2013, background): “Our recent study shows that Snail controls this glycolytic switch through repressing the fructose-1,6-biphosphatase (FBP1), a rate limiting enzyme in gluconeogenesis [109].”