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Axl as a potential therapeutic target for adamantinomatous craniopharyngiomas: Based on single nucleus RNA-seq and
Yiguang Chen1, Xiaohai Liu2, Yilamujiang Ainiwan3
1Department of Neurosurgery, Xuanwu Hospital Capital Medical University, Beijing, 100053, China; China International Neuroscience Institute (China-INI), Xuanwu Hospital, Capital Medical University, Beijing, 100053, China; Department of Neurosurgery, Nanfang Hospital, Southern Medical University, No. 1838, Guangzhou North Road, Guangzhou, Guangdong, 510515, China.
Abstract:
Craniopharyngiomas (CPs), particularly Adamantinomatous Craniopharyngiomas (ACPs), often exhibit a heightened risk of postoperative recurrence and severe complications of the endocrine and hypothalamic function. The primary objective of this study is to investigate potential novel targeted therapies within the microenvironment of ACP tumors. Cancer-Associated Fibroblasts (CAFs) were identified in the craniopharyngioma microenvironment, notably in regions characterized by cholesterol clefts, wet keratin, ghost cells, and fibrous stroma in ACPs. CAFs, alongside ghost cells, basaloid-like epithelium cells and calcifications, were found to secrete PROS1 and GAS6, which can activate AXL receptors on the surface of tumor epithelium cells, promoting immune suppression and tumor progression in ACPs. Additionally, the AXL inhibitor Bemcentinib effectively inhibited the proliferation organoids and enhanced the immunotherapeutic efficacy of Atezolizumab. Furthermore, neural crest-like cells were observed in the glial reactive tissue surrounding finger-like protrusions. Overall, our results revealed that the AXL might be a potentially effective therapeutic target for ACPs.
Insights
Adamantinomatous craniopharyngiomas (ACPs) involve cancer-associated fibroblasts secreting proteins that promote tumor growth. Targeting the AXL receptor shows promise for inhibiting ACP progression and enhancing immunotherapy.
Area of Science:
- Oncology
- Cancer Biology
- Tumor Microenvironment
Background:
- Adamantinomatous craniopharyngiomas (ACPs) frequently recur and cause severe endocrine/hypothalamic dysfunction.
- The tumor microenvironment's role in ACP progression remains incompletely understood.
Purpose of the Study:
- To explore novel targeted therapies within the ACP tumor microenvironment.
- To investigate the function of cancer-associated fibroblasts (CAFs) in ACPs.
Main Methods:
- Identification and characterization of CAFs within ACP tumor tissues.
- Analysis of protein secretion by CAFs and tumor cells (PROS1, GAS6).
- Assessment of AXL receptor activation and its downstream effects on tumor cells.
- Evaluation of AXL inhibitor (Bemcentinib) and immunotherapy (Atezolizumab) efficacy in vitro.
Main Results:
- CAFs were identified in ACPs, co-localizing with characteristic tumor features.
- CAFs and tumor cells secrete PROS1 and GAS6, activating AXL receptors on tumor epithelium.
- AXL activation promotes immune suppression and tumor progression in ACPs.
- Bemcentinib inhibited ACP organoid proliferation and enhanced Atezolizumab's efficacy.
Conclusions:
- The AXL signaling pathway is implicated in ACP progression and immune evasion.
- AXL represents a potential therapeutic target for Adamantinomatous Craniopharyngiomas.
- Combination therapy targeting AXL and immune checkpoints may improve treatment outcomes.
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