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Demethylation and Overexpression of CSF2 are Involved in Immune Response, Chemotherapy Resistance, and Poor Prognosis
Zongbin Xu1, Yiyi Zhang1, Meifang Xu2
1Department of Colorectal Surgery, Fujian Medical University Union Hospital, Fuzhou, People's Republic of China.
Purpose:
This study aimed to evaluate the role of colony-stimulating factor 2 (CSF2) in chemotherapy resistance, prognosis, and immune response and to identify its possible mechanisms underlying drug resistance.
Methods:
Drug-resistant cell lines were obtained by successively increasing drug concentration. RNA-Seq was performed to screen hub genes. CSF2 expression was analyzed via immunohistochemistry. Moreover, The Cancer Genome Atlas (TCGA), Tumor Immune Estimation Resource (TIMER) dataset, and R2 platform were used to explore the correlations among CSF2 expression, prognosis, and immune response.
Results:
RNA-Seq indicated that microRNAs in cancer, P53 signaling pathway, and cell cycle were associated with FOLFOX chemotherapy resistance. Protein-protein interaction (PPI), molecular complex detection (MOCDE), and qRT-PCR analysis verified CSF2 as the hub gene in chemotherapy resistance. Moreover, CSF2 expression was lower in the normal tissue than in the cancerous tissue (P<0.05). Higher expression of CSF2 was associated with poor OS and DFS in colon cancer patients (P<0.05). We further found similar results in the Oncomine database and R2 platform (P<0.05). A higher expression of CSF2 in the CRC tissue may be caused by demethylation, which was verified using the TCGA datasets. Moreover, GSEA demonstrated that CSF2 was associated with immune response, which was consistent with results reported using TIMER datasets.
Conclusion:
CSF2 is a novel biomarker and a prognostic factor for the survival of CRC patients affecting the immune response, and an overexpression of CSF2 in CRC patients may be caused by DNA demethylation.
Insights
Colony-stimulating factor 2 (CSF2) is identified as a key gene in chemotherapy resistance and a prognostic factor for colorectal cancer (CRC) patients, impacting immune response. Overexpression of CSF2 in CRC may stem from DNA demethylation.
Area of Science:
- Oncology
- Molecular Biology
- Immunology
Background:
- Chemotherapy resistance remains a significant challenge in colorectal cancer (CRC) treatment.
- Understanding the molecular mechanisms underlying drug resistance is crucial for improving patient outcomes.
- Colony-stimulating factor 2 (CSF2) has emerged as a potential factor influencing cancer progression and treatment response.
Purpose of the Study:
- To investigate the role of CSF2 in chemotherapy resistance in CRC.
- To evaluate CSF2 as a prognostic biomarker for CRC patient survival.
- To explore the association between CSF2 expression and the tumor immune microenvironment.
Main Methods:
- Drug-resistant cell lines were established and analyzed using RNA-Seq to identify key genes.
- CSF2 expression was assessed via immunohistochemistry and validated using TCGA, TIMER, and R2 datasets.
- Correlations between CSF2, prognosis (Overall Survival, Disease-Free Survival), and immune response were statistically analyzed.
Main Results:
- CSF2 was identified as a hub gene associated with FOLFOX chemotherapy resistance.
- Higher CSF2 expression correlated with poorer overall survival and disease-free survival in CRC patients.
- CSF2 expression was linked to immune response pathways, with overexpression potentially caused by DNA demethylation.
Conclusions:
- CSF2 serves as a novel biomarker and prognostic factor for CRC patient survival.
- CSF2 influences the immune response in colorectal cancer.
- DNA demethylation may contribute to CSF2 overexpression in CRC.
