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Characterization of morphological alterations in micropapillary adenocarcinoma of the lung

ABSTRACT: Characterization of morphological alterations in micropapillary adenocarcinoma of the lung

PROVIDER: PRJNA766741 | ENA |

REPOSITORIES: ENA

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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

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

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

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 |

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

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

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

| PRJNA1004218 | ENA

Comprehensive characterization of micropapillary colorectal adenocarcinoma.

Project description:Micropapillary colorectal adenocarcinoma is a morphologic subtype of colorectal cancer (CRC) with insufficiently characterized prognostic significance and biological features. We analyzed the histopathological, immunological, and prognostic features of micropapillary adenocarcinoma in two independent CRC cohorts (N = 1,876). We found that micropapillary adenocarcinomas accounted for 4.9% and 6.4% of CRCs in the two cohorts. A micropapillary growth pattern was associated with advanced stage and lymphovascular invasion (p < 0.001), but also with shorter overall survival independent of these factors and other prognostic parameters (Cohort 1: hazard ratio [HR] 1.76, 95% confidence interval [CI] 1.08-2.87; Cohort 2: HR 1.47, 95% CI 1.08-2.00). Multiplex immunohistochemistry and machine learning-assisted image analysis showed that the micropapillary growth pattern was associated with decreased CD3+ T-cell and CD14+HLA-DR+ monocytic cell densities. Molecular features of micropapillary adenocarcinoma were studied using bioinformatic analyses in The Cancer Genome Atlas (TCGA) cohort (N = 629) and validated with optical genome mapping and immunohistochemistry. These analyses revealed that micropapillary adenocarcinomas frequently present with chromosome region 8q24 copy number gain, TP53 mutation, and overexpression of UPK2, MUC16, and epithelial-mesenchymal transition involved genes, such as L1CAM. These results indicate that micropapillary colorectal adenocarcinoma is an aggressive morphologic subtype of CRC characterized by shorter overall survival, decreased antitumorigenic immune response, and unique molecular features. Our findings support the classification of micropapillary adenocarcinoma as a distinct, high-risk subtype of CRC, which should be systematically evaluated in patient care. © 2025 The Author(s). The Journal of Pathology published by John Wiley & Sons Ltd on behalf of The Pathological Society of Great Britain and Ireland.

| S-EPMC11880967 | biostudies-literature

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

| PRJNA1052743 | ENA

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

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