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A systematic dissection of the epigenomic heterogeneity of lung adenocarcinoma reveals two different subclasses with distinct prognosis and core regulatory networks [tumor]

ABSTRACT: Lung adenocarcinoma (LUAD) is a high malignant tumor mostly occurs in adult patients, which is also a highly heterogeneous disease that involved multi different alterations. Some alterations such like EGFR mutations are frequently observed in LUAD patients, but the mechanisms that drive LUAD tumorigenesis and progression remain largely unclear, which need further researches. For example, epigenetic processes play important roles in cancers, but the variations in the enhancer and super enhancer landscapes of LUAD patients have rarely been studied. Here, to provide an in-depth understanding of the epigenomic heterogeneity of LUAD, we investigate the H3K27ac histone modification profiles of the tumor and adjacent normal lung tissues from 42 LUAD patients and explore the role of epigenetic alterations in LUAD progression.

ORGANISM(S): Homo sapiens

PROVIDER: GSE150976 | GEO | 2020/05/22

REPOSITORIES: GEO

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A systematic dissection of the epigenomic heterogeneity of lung adenocarcinoma reveals two different subclasses with distinct prognosis and core regulatory networks [cell lines]

Project description:Lung adenocarcinoma (LUAD) is a high malignant tumor mostly occurs in adult patients, which is also a highly heterogeneous disease that involved multi different alterations. Some alterations such like EGFR mutations are frequently observed in LUAD patients, but the mechanisms that drive LUAD tumorigenesis and progression remain largely unclear, which need further researches. For example, epigenetic processes play important roles in cancers, but the variations in the enhancer and super enhancer landscapes of LUAD patients have rarely been studied. Here, to provide an in-depth understanding of the epigenomic heterogeneity of LUAD, we investigate the H3K27ac histone modification profiles of the tumor and adjacent normal lung tissues from 42 LUAD patients and explore the role of epigenetic alterations in LUAD progression.

2020-05-22 | GSE150975 | GEO

Epigenomic profiling and transcriptomic profiling of LUAD patients tumor tissues and tumor adjacent tissues

Project description:To provide an in-depth understanding of the epigenomic heterogeneity of LUAD, we here investigated the H3K27ac histone modification profiles of tumors and adjacent normal lung tissues from 42 LUAD patients and explored the role of epigenetic alterations in LUAD progression. We also investigated transcriptomic alterations among 36 patients tumor tissues.

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A novel lncRNA, LUADT1 promotes lung adenocarcinoma proliferation by epigenetic suppression of p27

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FAM111B contributes to the growth of lung adenocarcinoma with KRAS mutation by degrading p16 and promoting cell cycle.

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Project description:Lung adenocarcinoma (LUAD) remains a leading cause of cancer-related mortality worldwide. Understanding the dysregulated epigenetics governing LUAD progression is pivotal for identifying therapeutic targets. CBX4, a chromobox protein, is reported to be upregulated in LUAD. However, its regulatory role in LUAD progression warrants in-depth investigation. This study highlights the dual impact of CBX4 on LUAD proliferation and metastasis. Through a series of rigorous in vitro and in vivo experiments, we elucidate that CBX4 functions in promoting LUAD proliferation via upregulating PHGDH expression while concurrently suppressing LUAD metastasis by inhibiting ZEB2 transcription. Further investigation into the underlying mechanism reveals CBX4’s intricate interactions with distinct epigenetic factors. The inhibition of ZEB2 transcription involves CBX4-mediated recruitment of canonical PRC1 (cPRC1), establishing H2K119ub on the ZEB2 promoter. Simultaneously, CBX4 facilitates PHGDH transcription through interaction with GCN5, inducing heightened histone acetylation on the PHGDH promoter. These findings underscore CBX4's pivotal role as a regulator of LUAD progression, emphasizing its diverse transcriptional regulatory functions contingent upon interactions with specific epigenetic partners. Understanding the nuanced interplay between CBX4 and epigenetic factors sheds light on potential therapeutic avenues in LUAD.

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CBX4 in Lung Adenocarcinoma: A Dual-Edged Sword in Transcriptional Regulation and Tumor Progression [RNA-seq]

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Contextual epigenetic regulation of lung adenocarcinoma by GATA6 [RNA-Seq]

Project description:Lineage selective transcription factors (TFs) are important regulators of tumorigenesis, but their biological functions are often context dependent and their epigenetic mechanisms of action undefined. In this study, we uncover a conditional role for the endodermal and pulmonary specifying TF GATA6 during the initiation and progression of Kras mutant lung adenocarcinoma (LUAD). Inhibition of Gata6 in genetically engineered mouse models dampens the proliferation and increases the differentiation of LUAD tumors. These effects are influenced in part by the epithelial cell type that is targeted for transformation. In lung cancer cells derived from surfactant protein C expressing progenitors, we identify multiple genomic loci that are bound by GATA6. Moreover, suppression of Gata6 in these cells significantly alters chromatin accessibility, particularly at distal enhancer elements. Analogous to its paradoxical activity in the developing lungs, GATA6 expression fluctuates during different stages of LUAD progression and can control diverse lineage gene expression networks associated with cell proliferation, alveolar specification, BMP signaling, and epithelial plasticity. These findings demonstrate how GATA6 can broadly modulate the epigenome of lung tumor cells, which in turn may potentiate its divergent functions during cancer progression

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