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Updated: Sep 24, 2025

Transfer of Manipulated Tumor-associated Neutrophils into Tumor-Bearing Mice to Study their Angiogenic Potential In Vivo
Published on: July 20, 2019
SNF5 promotes cell proliferation and immune evasion in non-small cell lung cancer
Ying Chen1, Meilian Zhao1, Dongliang Shen1
1Key Laboratory of Biorheological Science and Technology, Ministry of Education, College of Bioengineering, Chongqing University, Chongqing, China.
Abstract:
Immune evasion is the process that tumor cells accelerate growth and metastasis by evading the recognition and attack of immune cells. SNF5 is one of the core subunits of SWI/SNF, which is involved in the development of a variety of malignancies. However, the functions of SNF5 in Non-Small Cell Lung Cancer (NSCLC) and the mechanism of SNF5 regulates immune evasion are still unclear. Based on this, we analyzed the expression of SNF5 and overall survival of lung cancer tissues through the cancer genome atlas (TCGA) database. Then we performed genetic gain and loss of function experiments with SNF5 using lentivirus infection and siRNA in NSCLC A549 and NCI-H1299 cells, respectively. We investigated the proliferation and immune evasion of these cells. We further explored the mechanism of SNF5 on NSCLC cells immune evasion. Our data showed that SNF5 was significantly increased in lung cancer tissues than that in normal lung tissues. Furthermore, SNF5 promoted NSCLC cells proliferation and the expressions of immune evasion-related genes. Meantime, overexpressed SNF5 reduced mortality of A549 cells when co-cultured with T cells. Moreover, SNF5 regulated the immune evasion by activating the signal transducer and activator of transcription (STAT3)/ phospho-STAT3 pathway in NSCLC cells. Together, our results validate SNF5 as a tumor oncogene and provide a new target for NSCLC treatment.
Insights
SNF5 promotes Non-Small Cell Lung Cancer (NSCLC) growth and immune evasion by activating the STAT3 pathway. This oncogene presents a potential therapeutic target for NSCLC treatment.
Area of Science:
- Oncology
- Immunology
- Molecular Biology
Background:
- Tumor cells use immune evasion to enhance growth and metastasis.
- SNF5, a SWI/SNF subunit, is implicated in malignancies, but its role in Non-Small Cell Lung Cancer (NSCLC) immune evasion is unknown.
Purpose of the Study:
- To investigate the function of SNF5 in NSCLC proliferation and immune evasion.
- To elucidate the mechanism by which SNF5 regulates immune evasion in NSCLC.
Main Methods:
- Analyzed SNF5 expression and survival in lung cancer using TCGA database.
- Performed gain and loss of function experiments in NSCLC cell lines (A549, NCI-H1299) using lentivirus and siRNA.
- Assessed cell proliferation, immune evasion gene expression, and co-culture with T cells.
- Explored the STAT3/phospho-STAT3 pathway activation.
Main Results:
- SNF5 expression is significantly elevated in lung cancer tissues compared to normal tissues.
- SNF5 overexpression promotes NSCLC cell proliferation and upregulates immune evasion genes.
- Overexpression of SNF5 reduces NSCLC cell mortality during co-culture with T cells.
- SNF5 activates the STAT3/phospho-STAT3 pathway, contributing to immune evasion.
Conclusions:
- SNF5 acts as an oncogene in NSCLC.
- SNF5 promotes NSCLC progression and immune evasion via the STAT3 pathway.
- SNF5 represents a promising therapeutic target for NSCLC treatment.
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