The DOI matches its Crossref record; 7 of the 7 references it cites were found in a registry or an index.
Na/K-ATPase Y260 Phosphorylation–mediated Src Regulation in Control of Aerobic Glycolysis and Tumor Growth
Open accessAbstract
We report here the identification of α1 Na/K-ATPase as a major regulator of the proto-oncogene Src kinase and the role of this regulation in control of Warburg effect and tumor growth. Specifically, we discovered Y260 in α1 Na/K-ATPase as a Src-specific phosphorylation and binding site and that Y260 phosphorylation is required for Src-mediated signal transduction in response to a number of stimuli including EGF. As such, it enables a dynamic control of aerobic glycolysis. However, such regulation appears to be lost or attenuated in human cancers as the expression of Na/K-ATPase α1 was significantly decreased in prostate, breast and kidney cancers, and further reduced in corresponding metastatic lesions in patient samples. Consistently, knockdown of α1 Na/K-ATPase led to a further increase in lactate production and the growth of tumor xenograft. These findings suggest that α1 Na/K-ATPase works as a tumor suppressor and that a loss of Na/K-ATPase-mediated Src regulation may lead to Warburg phenotype in cancer.
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Cites
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Metadata
- Authors
- Banerjee, M., Cui, X., Li, Z., Yu, H., Cai, L., Jia, X., He, D., Wang, C., Gao, T., & Xie, Z.
- Venue
- Scientific Reports
- Published
- 2018-08-17
- Volume
- 8
- Issue
- 1
- Pages
- 12322-12322
- ISSN
- 2045-2322 (ISSN-L)
- OpenAlex
- W2885531798
- Cited by
- 506
- References
- 7
- FWCI
- 32.58
- Type
- journal article
- Language
- en
- Open access
- gold
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- Banerjee, M., Cui, X., Li, Z., Yu, H., Cai, L., Jia, X., He, D., Wang, C., Gao, T., & Xie, Z. (2018). Na/K-ATPase Y260 Phosphorylation–mediated Src Regulation in Control of Aerobic Glycolysis and Tumor Growth. Scientific Reports. https://doi.org/10.1038/s41598-018-29995-2
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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