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Multiple Omics Analysis of the Role of RBM10 Gene Instability in Immune Regulation and Drug Sensitivity in Patients
Liusheng Wu1,2,3, Qi Liu3, Xin Ruan3
1Beijing Tsinghua Changgung Hospital, School of Clinical Medicine, Tsinghua University, Beijing 100084, China.
Objective:
The RNA-binding protein RBM10 can regulate apoptosis during the proliferation and migration of pancreatic cancer, endometrial cancer, and osteosarcoma cells; however, the molecular mechanism underlying lung adenocarcinoma is rarely reported. Recent studies have detected multiple truncated and missense mutations in RBM10 in lung adenocarcinoma, but the role of RBM10 in lung adenocarcinoma is unclear. This study mainly explored the immune regulation mechanism of RBM10 in the development of lung adenocarcinoma and its influence on sensitivity to targeted therapy drugs.
Methods:
The transcriptome data of CGAP were used to analyze the RNA-seq data of lung adenocarcinoma patients from different subgroups by using the CIBERSORT algorithm to infer the relative proportion of various immune infiltrating cells, and Spearman correlation analysis was performed to determine the gene expression and immune cell content. In addition, this study utilized drug trial data from the GDSC database. The IC50 estimates for each specific targeted therapy were obtained by using a regression method, and the regression and prediction accuracy were tested via ten cross-validations with the GDSC training set. An immunohistochemical test was performed on the samples of 20 patients with lung adenocarcinoma in the subcomponent analysis of immune cells, and the protein expression of RBM10 in lung adenocarcinoma tissues was verified by cellular immunofluorescence assays. Nucleic acids were extracted at low temperatures, and qRT-PCR was used to verify the expression levels of the mRNA of RBM10 in lung adenocarcinoma tissues and normal tissues (p < 0.05).
Results:
After screening and inclusion using a machine language, the results showed that RBM10 was significantly highly expressed in the lung adenocarcinoma tissues. The related signaling pathways were mainly concentrated in ncRNA processing, rRNA metabolic processes, ribosome biogenesis, and the regulation of translation. The qRT-PCR for 20 lung adenocarcinoma tissues showed that the expression of RBM10 in these tissues was significantly different from that in normal tissues (p = 0.0255). Immunohistochemistry analysis and cell immunofluorescence staining also confirmed that RBM10 was involved in the immune regulation of lung adenocarcinoma tissues, and the number of immune cell aggregations was significantly higher than that of the control group. RBM10 regulates B cell memory-CIBERSORT (p = 0.042) and B cell memory-CIBERSOTRT-abs (p = 0.027), cancer-associated fibroblast-EPIC (p = 0.001), cancer-associated fibroblast- MCPCounter (p = 0.0037), etc. The risk score was significantly associated with the sensitivity of patients to lapatinib (p = 0.049), nilotinib (p = 0.015), pazopanib (p = 0.001), and sorafenib (p = 0.048).
Conclusions:
RBM10 can inhibit the proliferation and invasion of lung adenocarcinoma cells through negative regulation and promote the apoptosis of lung adenocarcinoma cells through immunomodulatory mechanisms. The expression level of RBM10 affects the efficacy of targeted drug therapy and the survival prognosis of lung adenocarcinoma patients, which has a certain guiding significance for the clinical treatment of these patients.
Insights
The RNA-binding protein RBM10 inhibits lung adenocarcinoma progression and promotes apoptosis via immune regulation. Its expression impacts targeted therapy effectiveness and patient survival, offering clinical guidance.
Area of Science:
- Oncology
- Molecular Biology
- Immunology
Background:
- The RNA-binding protein RBM10's role in lung adenocarcinoma (LUAD) is under-explored, despite its known function in other cancers.
- Mutations in RBM10 have been identified in LUAD, suggesting a potential role in tumorigenesis.
Purpose of the Study:
- To investigate the immune regulatory mechanism of RBM10 in LUAD development.
- To determine the influence of RBM10 on sensitivity to targeted therapy drugs in LUAD.
Main Methods:
- Analysis of CGAP transcriptome data using CIBERSORT for immune cell infiltration.
- Spearman correlation analysis to link gene expression with immune cell content.
- Utilized GDSC database for drug sensitivity analysis and IC50 estimation.
- Immunohistochemistry and immunofluorescence assays to validate RBM10 protein expression.
- Quantitative real-time PCR (qRT-PCR) to confirm mRNA expression levels.
Main Results:
- RBM10 was significantly upregulated in LUAD tissues compared to normal tissues (p=0.0255).
- RBM10 expression correlated with immune cell infiltration, including B cell memory and cancer-associated fibroblasts.
- High RBM10 expression was associated with increased sensitivity to targeted therapies like lapatinib, nilotinib, pazopanib, and sorafenib.
Conclusions:
- RBM10 inhibits LUAD cell proliferation and invasion while promoting apoptosis through immunomodulatory mechanisms.
- RBM10 expression levels serve as a predictive biomarker for targeted therapy efficacy and patient prognosis in LUAD.
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