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

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

PROVIDER: PRJNA1052018 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27199374_1.fastq.gz	Fastqsanger.gz
	SRR27199374_2.fastq.gz	Fastqsanger.gz
	SRR27199375_1.fastq.gz	Fastqsanger.gz
	SRR27199375_2.fastq.gz	Fastqsanger.gz
	SRR27199376_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

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

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

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

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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

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

Proteomics analysis of different histologic subtypes of lung adenocarcinoma reveals a critical role of LRPAP1 in micropapillary pattern metastasis

Project description:Lung adenocarcinomas differ in prognosis based on their histologic growth pattern. Micropapillary growth in lung adenocarcinoma is associated with a host of adverse prognostic factors, especially metastases. Metastasis is the major cause of high mortality in lung cancer. Exploring the underlying mechanisms of metastasis in the early stage thus holds promise for identifying new therapeutic strategies that may enhance survival. We applied quantitative mass spectrometry to compare protein expression profiles in different histologic subtypes, including adenocarcinoma in situ (AIS), minimally invasive adenocarcinoma (MIA), invasive adenocarcinoma (IAC) histologic subtype includes acinar (ACI), micropapillary (MIP). We discovered that low-density lipoprotein receptor–related protein–associated protein 1 (LRPAP1) has the highest protein level in MIP, which was confirmed by immunohistochemistry (IHC). The co-expressed proteins in our data like PSMD1 and HSP90AB1 were also reported they are high-expressed in cancer and have important role in metastasis. Overexpressed LRPAP1 promoted migration of lung cancer cells in vitro. Our findings suggest that LRPAP1 plays an important role in promoting lung cancer cell metastasis, and may act as a novel target for anti-metastatic therapy.

2022-12-07 | PXD038594 |

Characterization of morphological alterations in micropapillary adenocarcinoma of the lung

Project description:Characterization of morphological alterations in micropapillary adenocarcinoma of the lung

| PRJNA766741 | 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

Gene expression profile of canine mammary malignancy

Project description:Molecular mechanisms of the canine mammary malignancy. RNA isolated from canine mammary tumours of the 3rd grade of malignancy was pooled and hybrydized on the same microarray as RNA isolated from canine mammary tumours of the 1st grade of malignancy. Based on the results the "malignancy portrait" was assessed. Dye-swap experiment, gene expression in the most malignant canine mammary tumours (the 3rd grade of malignancy) was compared to the less malignant tumours (1st grade of malignancy).

2013-10-01 | E-GEOD-44033 | biostudies-arrayexpress

Transcriptomic Analysis Of Micropapillary High Grade T1 Urothelial Bladder Cancer

Project description:Management of high-grade T1 (HGT1) micropapillary bladder cancer (MPBC) is controversial. An accurate genomic characterization might help predict outcome. We analyze the transcriptomic profile of MPBC in a clinically annotated HGT1 cohort establishing correlation with clinical outcome.A retrospective analysis of prospectively clinically followed series of HGT1; 23 patients with MPBC and 64 without MPBC (reference set). We identified a set of genes differentially expressed (DE). Associations between; clinical variables and gene expression (GE) levels (Wilcoxon’s rank sum); GE and time to progression (TTP) in univariate analysis (Log rank); GE levels adjusting for clinical variables (Cox regression) were evaluated.We identified a 26-gene signature that characterized MPBC in HGT1. Several genes including CD36, FAPB3 and RAETE1 were significantly associated with TTP. High expression of FABP3 and CD36 were associated with shorter TTP (P=0.045 and P=0.08 (NS)) as was low expression of RAET1E (P=0.01). Limitations include the lack of specific quantification of the percentage of MPBC tumor >10%.

2021-01-31 | GSE136401 | GEO

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