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The immune heterogeneity between pulmonary adenocarcinoma and squamous cell carcinoma: a comprehensive analysis based on lncRNA model

ABSTRACT: The immune heterogeneity between pulmonary adenocarcinoma and squamous cell carcinoma: a comprehensive analysis based on lncRNA model

PROVIDER: PRJNA745943 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15102218_1.fastq.gz	Fastqsanger.gz
	SRR15102218_2.fastq.gz	Fastqsanger.gz
	SRR15102219_1.fastq.gz	Fastqsanger.gz
	SRR15102219_2.fastq.gz	Fastqsanger.gz
	SRR15102220_1.fastq.gz	Fastqsanger.gz

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The immune heterogeneity between pulmonary adenocarcinoma and squamous cell carcinoma: a comprehensive analysis based on lncRNA model

Project description:Adenocarcinoma (AD) and squamous carcinoma (SCC) are major types of lung cancer. Although they both belong to non-small cell lung cancer (NSCLC), the differences in clinical prognosis and molecular mechanism between them are remarkable. Recently, numerous studies proved that immune status of carcinoma patients influence deeply the clinical outcome. Based on the theory of “Immune edit”, many immunotherapies come out and tremendously extended the life of the patients. Thus, research on immune status is significant and essential. Our study aims to select specific lncRNAs which control the key immune-related genes to construct the risk model for AD and SCC respectively and the patients were divided into high- and low-risk groups based on risk score. The prognostic significance of risk score was validated by our own cohorts. Besides, The GSEA analysis suggested that immune response or process of AD patients in high-risk group was weaken while the situation is opposite for SCC cohort. The evaluation of immune infiltration reveled that the infiltrating degree of dendritic cell (DC cell) might be the important change for AD patients. In addition, the prediction of response to immune checkpoint inhibitors (ICIs) treatment, based on T cell immune dysfunction and exclusion (TIDE) and immunophenoscore (IPS), indicated that the reasons for the deterioration of the immune microenvironment were T cell exclusion in AD patients and T cell dysfunction in SCC patients and the high-risk patients with SCC might benefit from ICIs treatment. Furthermore, the prediction of downstream targets via The Cancer Proteome Atlas (TCPA) database and RNA-seq analysis based on transferred lung cancer cell line indicated that lINC00996 was potential to become the therapeutic target for AD patients.

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Project description:Adenocarcinoma (AD) and squamous cell carcinoma (SCC) are both classified as major forms of non-small cell lung cancer, but differences in clinical prognoses and molecular mechanisms are remarkable. Recent studies have supported the importance of understanding immune status in that it influences clinical outcomes of cancer, and immunotherapies based on the theory of "immune editing" have had notable clinical success. Our study aimed to identify specific long non-coding (lnc) RNAs that control key immune-related genes and to use them to construct risk models for AD and SCC. Risk scores were used to separate patients into high- and low-risk groups, and we validated the prognostic significance of both risk scores with our own cohorts. A Gene Set Enrichment Analysis suggested that the immune responses of patients in the AD high-risk group and the SCC low-risk group tended to be weakened. Evaluation of immune infiltration revealed that the degree of infiltration of dendritic cells is of particular importance in AD. In addition, prediction of responses to immune checkpoint inhibitor (ICI) treatments, based on the T Cell Immune Dysfunction and Exclusion and immunophenoscore models, indicated that deterioration of the immune microenvironment is due mainly to T cell exclusion in AD patients and T cell dysfunction in SCC patients and that high-risk patients with SCC might benefit from ICI treatment. The prediction of downstream targets via The Cancer Proteome Atlas and RNA-seq analyses of a transfected lung cancer cell line indicated that the lncRNA LINC00996 is a potential therapeutic target in AD.

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