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p85β regulates autophagic degradation of AXL to activate oncogenic signaling
Ling Rao1, Victor C Y Mak1, Yuan Zhou1
1School of Biomedical Sciences, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong, Hong Kong.
Abstract:
PIK3R2 encodes the p85β regulatory subunit of phosphatidylinositol 3-kinase and is frequently amplified in cancers. The signaling mechanism and therapeutic implication of p85β are poorly understood. Here we report that p85β upregulates the protein level of the receptor tyrosine kinase AXL to induce oncogenic signaling in ovarian cancer. p85β activates p110 activity and AKT-independent PDK1/SGK3 signaling to promote tumorigenic phenotypes, which are all abolished upon inhibition of AXL. At the molecular level, p85β alters the phosphorylation of TRIM2 (an E3 ligase) and optineurin (an autophagy receptor), which mediate the selective regulation of AXL by p85β, thereby disrupting the autophagic degradation of the AXL protein. Therapeutically, p85β expression renders ovarian cancer cells vulnerable to inhibitors of AXL, p110, or PDK1. Conversely, p85β-depleted cells are less sensitive to these inhibitors. Together, our findings provide a rationale for pharmacological blockade of the AXL signaling axis in PIK3R2-amplified ovarian cancer.
Insights
Amplification of PIK3R2, encoding p85β, drives ovarian cancer by increasing AXL protein. Targeting AXL or related pathways offers a new therapeutic strategy for PIK3R2-amplified cancers.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Signaling
Background:
- PIK3R2 amplification is common in cancers, but its role in oncogenic signaling is unclear.
- The p85β regulatory subunit of phosphatidylinositol 3-kinase (PI3K) is implicated in cancer, yet its precise mechanisms and therapeutic relevance remain poorly understood.
Purpose of the Study:
- To elucidate the signaling mechanisms and therapeutic implications of p85β in ovarian cancer.
- To investigate how p85β contributes to oncogenesis and identify potential therapeutic targets.
Main Methods:
- Investigated the effect of p85β on receptor tyrosine kinase AXL levels and downstream signaling pathways.
- Utilized molecular biology techniques to examine the interplay between p85β, AXL, and autophagy-related proteins (TRIM2, optineurin).
- Assessed the sensitivity of ovarian cancer cells with varying p85β expression to inhibitors of AXL, PI3K (p110), and PDK1.
Main Results:
- p85β upregulates AXL protein levels, promoting oncogenic signaling in ovarian cancer.
- p85β activates AKT-independent PDK1/SGK3 signaling and disrupts autophagic degradation of AXL via TRIM2 and optineurin.
- p85β expression sensitizes ovarian cancer cells to AXL, p110, or PDK1 inhibitors, while p85β depletion reduces sensitivity.
Conclusions:
- p85β drives ovarian cancer progression by stabilizing AXL and activating specific signaling pathways.
- Pharmacological inhibition of the AXL signaling axis is a promising therapeutic strategy for PIK3R2-amplified ovarian cancers.
- Understanding the p85β-AXL interaction provides a rationale for targeted therapies in specific cancer subtypes.
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