What question did this study set out to answer?

To investigate the molecular mechanisms by which macrophages and inflammatory TNFα signaling promote breast cancer cell migration and metastatic progression.

September 25, 2017OncogenesisOpen Access

TNFα-YAP/p65-HK2 axis mediates breast cancer cell migration

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To investigate the molecular mechanisms by which macrophages and inflammatory TNFα signaling promote breast cancer cell migration and metastatic progression.
Exposed breast cancer cells to macrophage-conditioned medium and TNFα to examine alterations in cellular migration and intracellular signaling pathways.
Performed chromatin immunoprecipitation assays to evaluate whether transcription factors YAP, TEAD, and p65 directly bind and regulate metabolic target genes.
Macrophage-conditioned medium and TNFα induced IKK-mediated YAP phosphorylation, activation, and increased physical interaction with p65 in breast cancer cells.
YAP/TEAD and p65 synergistically activated transcription of hexokinase 2 (HK2), the rate-limiting enzyme in glycolysis, thereby driving inflammation-induced cell migration.

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Implication

Mechanistic study reveals that TNFα drives breast cancer cell migration via an IKK-YAP/p65-HK2 signaling axis, highlighting a key molecular link between tumor inflammation and metastasis.

Cite This Study

Gao et al. (2017) studied this question.

synapsesocial.com/papers/6a7eb687e26ba2240a9a15d4 https://doi.org/10.1038/oncsis.2017.83

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Implication

Mechanistic study reveals that TNFα drives breast cancer cell migration via an IKK-YAP/p65-HK2 signaling axis, highlighting a key molecular link between tumor inflammation and metastasis.

TNFα-YAP/p65-HK2 axis mediates breast cancer cell migration

Key Points

Discussion

Implication

Cite This Study

TNFα-YAP/p65-HK2 axis mediates breast cancer cell migration

Key Points

Discussion

Implication

Cite This Study

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