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From man to mouse and back again: advances in defining tumor AKTivities in vivo
David F Restuccia1, Brian A Hemmings
1Friedrich Miescher Institute for Biomedical Research, Maulbeerstrasse 66, CH-4058 Basel, Switzerland. david.restuccia@fmi.ch
Abstract:
AKT hyperactivation is a common event in human cancers, and inhibition of oncogenic AKT activation is a major goal of drug discovery programs. Mouse tumor models that replicate AKT activation typical of human cancers provide a powerful means by which to investigate mechanisms of oncogenic signaling, identify potential therapeutic targets and determine treatment regimes with maximal therapeutic efficacy. This Perspective highlights recent advances using in vivo studies that reveal how AKT signaling supports tumor formation, cooperates with other mutations to promote tumor progression and facilitates tumor-cell dissemination, focusing on well-characterized prostate carcinoma mouse models that are highly sensitive to AKT activation. The implications of these findings on the therapeutic targeting of AKT and potential new drug targets are also explored.
Insights
Targeting AKT signaling, crucial in many cancers, is a key drug discovery goal. Mouse models reveal how AKT drives tumor growth, progression, and spread, informing new cancer therapies.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- AKT hyperactivation is prevalent in human cancers.
- Inhibiting oncogenic AKT is a critical objective in cancer drug discovery.
- Mouse tumor models are essential for studying AKT-driven oncogenesis.
Purpose of the Study:
- To review recent in vivo studies on AKT signaling in cancer.
- To highlight the role of AKT in tumor formation, progression, and metastasis.
- To explore therapeutic strategies targeting AKT in prostate cancer models.
Main Methods:
- Analysis of in vivo studies using mouse tumor models.
- Focus on well-characterized prostate carcinoma models sensitive to AKT activation.
- Review of findings related to oncogenic AKT signaling mechanisms.
Main Results:
- AKT signaling supports tumor formation and progression.
- AKT cooperates with other mutations to drive cancer advancement.
- AKT facilitates tumor cell dissemination and metastasis.
- Prostate carcinoma mouse models are highly sensitive to AKT activation.
Conclusions:
- In vivo studies provide insights into AKT's role in cancer.
- Understanding AKT mechanisms can identify new therapeutic targets.
- Targeting AKT is a promising strategy for cancer treatment, particularly in prostate cancer.
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