RUNX2 and the PI3K/AKT axis reciprocal activation as a driving force for tumor progression

Karine A. Cohen-Solal, Rajeev K. Boregowda, Ahmed Lasfar

    Research output: Contribution to journalReview articlepeer-review

    74 Scopus citations


    From the first reported role of the transcription factor RUNX2 in osteoblast and chondrocyte differentiation and migration to its involvement in promigratory/proinvasive behavior of breast, prostate, and thyroid cancer cells, osteosarcoma, or melanoma cells, RUNX2 currently emerges as a key player in metastasis. In this review, we address the interaction of RUNX2 with the PI3K/AKT signaling pathway, one of the critical axes controlling cancer growth and metastasis. AKT, either by directly phosphorylating/activating RUNX2 or phosphorylating/inactivating regulators of RUNX2 stability or activity, contributes to RUNX2 transcriptional activity. Reciprocally, the activation of the PI3K/AKT pathway by RUNX2 regulation of its different components has been described in non-transformed and transformed cells. This mutual activation in the context of cancer cells exhibiting constitutive AKT activation and high levels of RUNX2 might constitute a major driving force in tumor progression and aggressiveness.

    Original languageEnglish (US)
    Article number137
    JournalMolecular Cancer
    Issue number1
    StatePublished - Jul 25 2015

    All Science Journal Classification (ASJC) codes

    • Molecular Medicine
    • Oncology
    • Cancer Research


    • Invasion
    • Migration
    • Phosphatidylinositol 3-kinase (PI3K)
    • Protein Kinase B (PKB/AKT)
    • RUNX2
    • Transcription factor


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