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MYC recruits tumor-associated macrophage to sustain metastatic malignancy of lung adenocarcinoma micropapillary subtype through epigenetic reprogramming

ABSTRACT: MYC recruits tumor-associated macrophage to sustain metastatic malignancy of lung adenocarcinoma micropapillary subtype through epigenetic reprogramming

PROVIDER: PRJNA1052743 | ENA |

REPOSITORIES: ENA

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MYC recruits tumor-associated macrophage to sustain metastatic malignancy of lung adenocarcinoma micropapillary subtype through epigenetic reprogramming

Project description:Current comprehension of micropapillary lung adenocarcinoma (MP-LUAD) remains circumscribed to the realms of biological behaviors and genomic landscapes. Previous studies from our institute have shown that there exist subtle and unactionable genomic alterations between MP and non-MP early-stage lung adenocarcinoma (LUAD). Therefore, deciphering the unknown non-genomic regulatory network of MP-pattern malignancy may offer opportunities to uncover more tractable therapeutic targets for MP-LUAD patients.Bulk RNA-seq after microdissection showed aberrant activation of the MYC pathway in MP. The CDX mouse model showed that MYC overexpression induced a MP-pattern malignancy in tumor tissues, but in vitro experiments lacked consistency. Through screening via single-cell RNA-se, retrospective cohort and TCGA dataset, we found aberrant accumulation of tumor-associated macrophages (TAMs) around MP tissues. in vitro co-culture and in vivo dependency experiments demonstrated that MYC overexpression in tumor cells exhibited a MP-pattern malignancy in collaboration with TAMs. Follow-up experiments revealed that, MYC interacts with the pioneer transcription factor FOSL2 induced by TGFβ secreted from TAMs, transcriptionally regulating the expression of MP-pattern genes.Our study uncovered copy number amplification-induced activation of MYC in MP-LUAD, which by recruiting TAMs, cooperatively transcriptionally regulates MP pattern genes and promotes a metastatic malignancy.

2025-04-02 | GSE250253 | GEO

Redundant MYC orchestrates M2-like macrophages induced chromatin remodeling to sustain micropapillary-pattern malignancy in Lung Adenocarcinoma

Project description:Current comprehension of micropapillary (MP)-subtype lung adenocarcinoma (LUAD) remains circumscribed to biological behaviors and genomic landscapes. Unraveling the core regulatory programs underlying MP-pattern malignancy offers opportunities to identify more feasible therapeutic targets for patients with MP-LUAD. We show aberrant activation of the MYC pathway in MP-subtype LUAD compared with other subtypes. MP-pattern malignancy cannot be solely induced by aberrant MYC expression in vitro or xenograft mouse models but requires the assistance of M2-like macrophages to accomplish. Redundantly expressed MYC aggregates M2-like macrophages derived from the bone marrow to secrete TGFβ, inducing the expression of FOSL2 in tumor cells, thereby remodeling chromatin accessibility in MP-pattern gene promoters to assist MYC in occupying de novo transcriptional regulation. Moreover, effective alleviation of MP-pattern malignancy can be achieved by disrupting the TGFβ-FOSL2 axis. These findings elucidate functions of M2-like macrophage-TGFβ-FOSL2 axis in MYC-redundant MP-subtype LUAD, defining targetable vulnerabilities.

2025-04-02 | GSE250097 | GEO

Redundant MYC orchestrates M2-like macrophages induced chromatin remodeling to sustain micropapillary-pattern malignancy in Lung Adenocarcinoma

Project description:Redundant MYC orchestrates M2-like macrophages induced chromatin remodeling to sustain micropapillary-pattern malignancy in Lung Adenocarcinoma

| PRJNA1052018 | ENA

Characterization of morphological alterations in micropapillary adenocarcinoma of the lung

Project description:Micropapillary adenocarcinoma of the lung is a cancer with poor prognosis and characterized by the presence of tumor cells with ring-like glandular structure floating within alveolar spaces. We investigated the association between its morphological, biochemical, and immunohistochemical characteristics and malignancy using the KU-Lu-MPPt3 cell line established from a patient with micropapillary adenocarcinoma. Two subpopulations of KU-Lu-MPPt3 cells, adhesive (AD) and clumpy and suspended (CS) cells, were prepared and subjected to DNA microarray.

2021-09-28 | GSE184883 | GEO

Gene expression profile of micropapillary bladder cancer

Project description:Analyses of mRNA gene expression profiling performed on 43 micropapillary bladder samples and 89 conventional urothelial carcinoma samples. Micropaillary tumors showed downregulation of miR-296 and activation of chromatin-remodeling complex RUVBL1. Micropapillary tumors evolve through luminal pathway.

2016-09-03 | GSE86411 | GEO

Association of frequent hypermethylation with high grade histological subtype in lung adenocarcinoma. (Infinium MethylationEPIC)

Project description:Comprehensive DNA methylation analysis of each histological LUAD subtype. Infinium MethylationEPIC BeadChip was used to obtain DNA methylation profiles across 850,000 CpG sites. Samples included 4 Micropapillary subtype, 5 Acinar subtype, 5 Solid subype.

2023-09-11 | GSE217731 | GEO

Association of frequent hypermethylation with high grade histological subtype in lung adenocarcinoma. (Infinium Methylation450K)

Project description:Comprehensive DNA methylation analysis of each histological LUAD subtype. Infinium HumanMethylation450 BeadChip was used to obtain DNA methylation profiles across 485,577 CpG sites. Samples included 6 Micropapillary subtype, 5 Papillary subtype, 5 Lepidic subype and 3 normal lung tissues.

2023-09-11 | GSE217732 | GEO

Hypoxia drives the formation of lung micropapillary adenocarcinoma through hypoxia-inducible factor-1a (RNA-seq)

Project description:Micropapillary adenocarcinoma (MPC) is an aggressive histologic subtype of lung adenocarcinoma (LUAD). MPC is composed of small clusters of cancer cells exhibiting inverted polarity. However, the mechanism underlying its formation is poorly understood. Here we show that hypoxia is involved in MPC formation. Spatial transcriptome analysis with human LUAD tissue suggested that hypoxia-inducible factor (HIF)-1 signaling is activated in MPC. Hypoxia induced the formation of MPC-like structures (MLSs) with inverted polarity in a three-dimensional culture system using A549 human LUAD cells, and HIF-1α was indispensable for MLS formation. RNA sequencing analysis demonstrated that A549 cells forming MLSs exhibited a gene expression signature similar to that of lung MPC. Moreover, MLS formation enhanced the resistance of A549 cells to natural killer cell cytotoxicity. Our findings suggest that hypoxia drives lung MPC formation through HIF-1α and that immune escape from natural killer cells might underlie the aggressiveness of MPC.

2025-01-08 | GSE240551 | GEO

H1N1 subtype

Project description:H1N1 subtype

| PRJNA477707 | ENA

Transcriptomic Analysis Of Micropapillary High Grade T1 Urothelial Bladder Cancer

Project description:Transcriptomic Analysis Of Micropapillary High Grade T1 Urothelial Bladder Cancer

| PRJNA562495 | ENA