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Single-cell RNA sequencing for the identification of early-stage lung cancer biomarkers from circulating blood

ABSTRACT: To develop biomarkers for diagnosis of early-stage lung adenocarcinoma (LUAD) patients, we set up single-cell RNA sequencing (scRNA-seq) pipeline using Fluidigm C1 systems. Through the scRNA-seq pipeline, we clustered 1,441 single cells from four non-small cell lung cancer (NSCLC) cell lines (A549, H460, H1299 and Calu3) into four groups based on differential gene expression and detected over 2,400 differentially expressed genes (DEGs) from a comparison of four clusters following dimension reduction. We validated fold change values of 120 DEGs selected from three cluster comparisons (top 20 up- and top 20 down-regulated genes per cluster comparison) using qRT-PCR approach. We performed further quantitative validation of chemokine genes (CXCL1 and CXCL2 with corresponding receptor, CXCR2) at mRNA level in tumour and tumour-adjacent normal lung tissues of LUAD patients (16 female and 19 male). Next, we profiled microRNAs epigenetically regulating expression of those chemokine genes in the tumour and normal tissues as well as blood (plasma) samples from corresponding LUAD patients. Finally, we identified relatively high copy number of miR-532-5p regulating those chemokine genes in patient plasma samples.

ORGANISM(S): Homo sapiens

PROVIDER: GSE183590 | GEO | 2021/09/14

REPOSITORIES: GEO

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Integrative multi-omic analysis of the SWI/SNF complex defines a new clinical subgroup of lung adenocarcinoma patients

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Project description:Lung adenocarcinoma (LUAD) is one of the deadliest malignancies worldwide. Dynamic lineage changes within the lung epithelium and the high plasticity of these epithelial cells confound the correct identification of the cell-of-origin of LUAD. Here, we combined lineage-tracing mouse models with an autochthonous cell type-independent LUAD model in order to discover the cellular origin of ALK-translocated LUAD. We identified Club and AT2 cells as the cells-of-origin of LUAD. Moreover, we uncovered epigenetic imprints in the tumours originating from Club or AT2 cells by whole-genome bisulfite sequencing. Single-cell transcriptomes of Club cells at different stages of tumour development identified two trajectories of Club cell evolution. On both routes, tumours lose their Club cell identity and gain an AT2-like phenotype. Together, this study highlights the role of Club cells in LUAD initiation and unveils key mechanisms conferring LUAD heterogeneity.

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Club cells employ regeneration mechanisms during lung tumorigenesis

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Transcriptomic Alterations in Lung Adenocarcinoma Unveil New Mechanisms Targeted by the TBX2 Subfamily of Tumor Suppressor Genes

Project description:T-box (TBX) transcription factors are evolutionary conserved genes and master transcriptional regulators. In mammals, TBX2 subfamily (TBX2, TBX3, TBX4, and TBX5) genes are expressed in the developing lung bud and tracheae. Our group previously showed that the expression of TBX2 subfamily was significantly high in human normal lungs, but markedly suppressed in lung adenocarcinoma (LUAD). To further elucidate their role in LUAD pathogenesis, we first confirmed abundant expression of protein products of the four members by immunostaining in adult human normal lung tissues. We also found overall suppressed expression of these genes and their corresponding proteins in a panel of human LUAD cell lines. Transient over-expression of each of the genes in human (NCI-H1299), and mouse (MDA-F471) derived lung cancer cells was found to significantly inhibit growth and proliferation as well as induce apoptosis. Genome-wide transcriptomic analyses on NCI-H1299 cells, overexpressing TBX2 gene subfamily, unraveled novel regulatory pathways. These included, among others, inhibition of cell cycle progression but more importantly activation of the histone demethylase pathway. When using a pattern-matching algorithm, we showed that TBX's overexpression mimic molecular signatures from azacitidine treated NCI-H1299 cells which in turn are inversely correlated to expression profiles of both human and murine lung tumors relative to matched normal lung. In conclusion, we showed that the TBX2 subfamily genes play a critical tumor suppressor role in lung cancer pathogenesis through regulating its methylating pattern, making them putative candidates for epigenetic therapy in LUAD.

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