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Assessing Cellular Target Engagement by SHP2 (PTPN11) Phosphatase Inhibitors
Published on: July 17, 2020
The p110delta isoform of PI 3-kinase negatively controls RhoA and PTEN
Evangelia A Papakonstanti1, Anne J Ridley, Bart Vanhaesebroeck
1Ludwig Institute for Cancer Research, London, UK.
Abstract:
Inactivation of PI 3-kinase (PI3K) signalling is critical for tumour suppression by PTEN. This is thought to be a unidirectional relationship in which PTEN degrades the lipids produced by PI3K, thus controlling cell proliferation, survival and migration. We now show that this relationship is in fact bidirectional, whereby PI3K reciprocally controls PTEN. We report that the p110delta PI3K negatively regulates PTEN, through a pathway involving inhibition of RhoA. Inactivation of p110delta in macrophages led to reduced Akt and Rac1 activation, but paradoxically to increased RhoA and PTEN activity. Partial inactivation of p190RhoGAP and a reduced binding of cytoplasmic RhoA to the cyclin-dependent kinase inhibitor p27 both contributed to the increased RhoA-GTP levels upon p110delta inactivation. Pharmacological inhibition of ROCK, a downstream effector kinase of RhoA, restored all signalling and functional defects of p110delta inactivation, including Akt phosphorylation, chemotaxis and proliferation. This work identifies the RhoA/ROCK pathway as a major target of p110delta-mediated PI3K signalling, and establishes for the first time that PI3K controls itself, via a feedback loop involving PTEN.
Insights
The PI3K/PTEN pathway, crucial for tumor suppression, is bidirectional. PI3K signaling reciprocally controls PTEN activity through the RhoA/ROCK pathway, revealing a novel feedback loop.
Area of Science:
- Cellular Biology
- Molecular Oncology
- Signal Transduction
Background:
- Phosphoinositide 3-kinase (PI3K) signaling is vital for tumor suppression, primarily through the action of PTEN.
- The PTEN-PI3K interaction was considered unidirectional, with PTEN lipid degradation controlling cell functions.
Purpose of the Study:
- To investigate the reciprocal regulation between PI3K and PTEN.
- To elucidate the role of PI3K in controlling PTEN activity and cellular processes.
Main Methods:
- Investigated the impact of p110delta PI3K inactivation in macrophages.
- Analyzed signaling pathways involving RhoA, Akt, Rac1, and PTEN.
- Utilized pharmacological inhibition of ROCK (a RhoA effector kinase).
Main Results:
- Inactivation of p110delta PI3K led to increased RhoA and PTEN activity, despite reduced Akt and Rac1 activation.
- Increased RhoA-GTP levels were linked to p190RhoGAP inactivation and reduced RhoA binding to p27.
- ROCK inhibition reversed signaling defects, including Akt phosphorylation, chemotaxis, and proliferation.
Conclusions:
- The PI3K/PTEN relationship is bidirectional, with PI3K negatively regulating PTEN via the RhoA/ROCK pathway.
- Identifies the RhoA/ROCK pathway as a key mediator of p110delta PI3K signaling.
- Establishes a novel feedback loop where PI3K controls itself through PTEN regulation.
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