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RUVBL1-mediated mTORC1 activation drives tumour progression and immune evasion for oral squamous cell carcinoma
Xinpei Wang1, Zuxuan Zhao2, Fengyang Jing3
1Department of Pathology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100021, China; Department of Oral Pathology, Peking University School and Hospital of Stomatology, National Center for Stomatology, National Clinical Research Center for Oral Diseases, National Engineering Research Center of Oral Biomaterials and Digital Medical Devices, Beijing, 100081, China; Research Unit of Precision Pathologic Diagnosis in Tumors of the Oral and Maxillofacial Regions, Chinese Academy of Medical Sciences, Beijing, 100081, China.
Background And Aims:
Oral squamous cell carcinoma (OSCC) is a prevalent head and neck malignancy for which surgical resection remains the primary therapeutic approach. Although immunotherapy, particularly immune checkpoint blockade targeting PD-1/PD-L1, has been revolutionary, only a small number of patients with OSCC have clinically benefited from it. Therefore, elucidating the molecular mechanisms underlying OSCC progression and immune evasion is crucial. RuvB-like AAA ATPase 1 (RUVBL1) has been implicated in diverse biological processes and modulates tumour immunity. Little is known regarding the function of RUVBL1 and its mechanism of action in OSCC. In this study, we aimed to understand RUVBL1 regulation in OSCC tissues and how expression correlates with patient prognosis.
Materials And Methods:
We conducted bioinformatics analysis, functional assays in vitro, co-culture experiments, and murine xenograft models, along with validation in clinical samples. To investigate the underlying mechanism, transcriptome sequencing and biochemical as well as molecular analyses were utilized.
Key Findings:
RUVBL1 promotes tumour growth and regulates the tumour microenvironment by controlling PD-L1 expression by targeting the rapamycin kinase (mTOR) pathway, thereby impairing both the infiltration and effector function of T cells in OSCC. Pharmacological inhibition of RUVBL1 with CB6644 suppressed tumour growth and synergised with PD-L1 blockade and conventional therapy. Collectively, these findings identify RUVBL1 as a critical driver of OSCC progression and immune modulation.
Significance:
Our findings highlight the potential of RUVBL1 as a prognostic biomarker and therapeutic target to enhance treatment efficacy.
Insights
RuvB-like AAA ATPase 1 (RUVBL1) drives oral squamous cell carcinoma (OSCC) growth and immune evasion by regulating PD-L1. Inhibiting RUVBL1 shows promise as a therapeutic strategy for OSCC treatment.
Area of Science:
- Oncology
- Immunology
- Molecular Biology
Background:
- Oral squamous cell carcinoma (OSCC) is a common head and neck cancer with limited treatment benefits from current immunotherapy.
- Understanding OSCC progression and immune evasion mechanisms is critical for improving patient outcomes.
- RuvB-like AAA ATPase 1 (RUVBL1) is involved in cellular processes and tumor immunity, but its role in OSCC is unclear.
Purpose of the Study:
- To investigate the regulation and function of RUVBL1 in OSCC.
- To determine the correlation between RUVBL1 expression and patient prognosis in OSCC.
- To elucidate the mechanism by which RUVBL1 influences the tumor microenvironment and immune response in OSCC.
Main Methods:
- Bioinformatics analysis, in vitro functional assays, co-culture experiments, and murine xenograft models were employed.
- Transcriptome sequencing, biochemical, and molecular analyses were utilized to investigate mechanisms.
- Clinical samples were used for validation of findings.
Main Results:
- RUVBL1 promotes OSCC tumor growth and modulates the tumor microenvironment by controlling PD-L1 expression via the mTOR pathway.
- RUVBL1 impairs T cell infiltration and effector function in OSCC.
- Pharmacological inhibition of RUVBL1 suppressed tumor growth and synergized with PD-L1 blockade and conventional therapy.
Conclusions:
- RUVBL1 is identified as a key driver of OSCC progression and immune modulation.
- RUVBL1 holds potential as a prognostic biomarker for OSCC.
- Targeting RUVBL1 presents a therapeutic strategy to enhance treatment efficacy in OSCC.
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