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RPL22 Expression Identifies a Transcriptional Subset of MLH1 Deficient Endometrial Cancers that Impacts Tumor Infiltrating Lymphocytes [protein]

ABSTRACT: RPL22 expression is lost is ~30% of MSI-high endometrial cancers, and the consequences of RPL22 loss are still unknown. The purpose of this study was to determine the consequences of RPL22 loss in both the tumor and immune microenvironment of MSI-high endometrial cancers. We determined that the number of CD8+ T cells in RPL22 negative tumors is significantly lower than in RPL22 positive tumors and that beta-2-microglobulin protein is significantly reduced in RPL22 negative tumors.

ORGANISM(S): Homo sapiens

PROVIDER: GSE302839 | GEO | 2025/12/10

REPOSITORIES: GEO

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RPL22 Expression Identifies a Transcriptional Subset of MLH1 Deficient Endometrial Cancers that Impacts Tumor Infiltrating Lymphocytes [transcript]

Project description:RPL22 expression is lost is ~30% of MSI-high endometrial cancers, and the consequences of RPL22 loss are still unknown. The purpose of this study was to determine the consequences of RPL22 loss in both the tumor and immune microenvironment of MSI-high endometrial cancers. We determined that the number of CD8+ T cells in RPL22 negative tumors is significantly lower than in RPL22 positive tumors and thatRPL22 positive tumors have distinct transcriptional profiles characterized by upregulation of immune pathways.

2025-12-10 | GSE302749 | GEO

RPL22 is a tumor suppressor in MSI-high cancers and a key splicing regulator of MDM4

Project description:Microsatellite instability high (MSI-H) tumors are malignant tumors that, despite harboring a high mutational burden, often have intact TP53. One of the most frequent mutations in MSI-H tumors is a frameshift mutation in RPL22, a ribosomal protein. Here, we identified RPL22 as a modulator of MDM4 splicing through an alternative splicing switch in exon 6. RPL22 loss increased MDM4 exon 6 inclusion, cell proliferation, and augmented resistance to the MDM inhibitor Nutlin-3A. RPL22 represses expression of its paralog, RPL22L1, by mediating the splicing of a cryptic exon corresponding to a truncated transcript. Therefore, RPL22 loss is a driver of oncogenic MDM4 induction and key to a common splicing circuit in MSI-H tumors that may inform therapeutic targeting of the MDM4-p53 axis and oncogenic RPL22L1 induction.

2024-07-22 | GSE263237 | GEO

RPL22 Expression Identifies a Transcriptional Subset of MLH1 Deficient Endometrial Cancers that Impacts Tumor Infiltrating Lymphocytes

Project description:RPL22 Expression Identifies a Transcriptional Subset of MLH1 Deficient Endometrial Cancers that Impacts Tumor Infiltrating Lymphocytes

| PRJNA1292250 | ENA

RPL22 Expression Identifies a Transcriptional Subset of MLH1 Deficient Endometrial Cancers that Impacts Tumor Infiltrating Lymphocytes [protein]

Project description:RPL22 Expression Identifies a Transcriptional Subset of MLH1 Deficient Endometrial Cancers that Impacts Tumor Infiltrating Lymphocytes [protein]

| PRJNA1292251 | ENA

RPL22 is a tumor suppressor in MSI-high cancers and a key splicing regulator of MDM4

Project description:RPL22 is a tumor suppressor in MSI-high cancers and a key splicing regulator of MDM4

| PRJNA1096328 | ENA

Cell-type specific gene expression profiling in heterogeneous in vitro cultures using epitope-tagged RPL22

Project description:Here we report the use of RPL22-Flag, RPL22-V5, and RPL22-HA to co-immunoprecipitate RNA from specific cell populations

2020-05-01 | GSE149076 | GEO

CRISPR screening identifies nucleolar RPL22 as a heterochromatin destabilizer and senescence driver

Project description:Dysfunction of the ribosome manifests during cellular senescence and contributes to tissue aging, functional decline, and development of aging-related disorders in ways that have remained enigmatic. Here, we conducted a comprehensive CRISPR-based loss-of-function (LOF) screen of ribosome-associated genes (RAGs) in human mesenchymal progenitor cells (hMPCs). Through this approach, we identified ribosomal protein L22 (RPL22) as the foremost RAG whose deficiency mitigates the effects of cellular senescence. Consequently, absence of RPL22 delays hMPCs from becoming senescent, while an excess of RPL22 accelerates the senescence process. Mechanistically, we found in senescent hMPCs, that RPL22 accumulates within the nucleolus. This accumulation triggers a cascade of events, including heterochromatin decompaction with concomitant degradation of key heterochromatin proteins, specifically heterochromatin protein 1γ (HP1γ) and heterochromatin protein KRAB-associated protein 1 (KAP1). Subsequently, RPL22-dependent breakdown of heterochromatin stimulates the transcription of ribosomal RNAs (rRNAs), triggering cellular senescence. In summary, our findings unveil a novel role for nucleolar RPL22 as a destabilizer of heterochromatin and a driver of cellular senescence, shedding new light on the intricate mechanisms underlying the aging process.

2024-02-14 | GSE253231 | GEO

The clinicopathological characteristics, prognosis and immune microenvironment mapping in MSI-H/MMR-D endometrial carcinomas

Project description:Endometrial cancer had a relatively high prevalence of MMR deficiency. MMR-D/MSI-H endometrial cancer patients are suggested to be potential beneficiaries of PD-1/PD-L1 inhibitor therapy. Here, we explored the prognostic value of MSI subtype in endometrial cancer and its correlation with immune environment. Based on expression and clinical data of 78 POLE, 123 MSI and 299 Other EC samples from the TCGA-UCEC project, we found that the MSI tumors were identified more often in early stage, had a lower age, better patient survival, enriched CD8+ T cells, and regulatory T cells and less M2 macrophages and activated dendritic cells than the Other group, and shared a relatively similar expression profile with POLE group by differential analysis. In addition, we established the immune landscape of an MMR-D endometrial cancer tissue using unbiased single-cell RNA-seq analysis of 3371 cells. By immunohistochemistry analysis, we found that the MMR-D tumors showed a higher trend of CD20+ B cells infiltration. Our study might expand our understanding of the role of immune subsets in MSI endometrial carcinomas and provide guidance of immunotherapy for endometrial cancer.

2022-03-09 | GSE193430 | GEO

A Proteogenomic View of Synchronous Endometrioid Endometrial and Ovarian Cancer

Project description:Purpose: Increasing genomics-based evidence suggests that synchronous endometrial and ovarian cancer (SEOC) represents clonally related primary and metastatic tumors. A systematic analysis of the global protein landscape of SEOCs, heretofore lacking, could reveal functional and disease-specific consequences of known genetic alterations, the directionality of metastasis, and accurate histological markers to distinguish SEOCs from single-site tumors. Experimental Design: We performed a systematic proteogenomic analysis of 29 patients diagnosed with SEOC at three international gynecologic oncology treatment centers (Chicago, Vancouver, Tübingen). For direct comparison to single-site tumors, we included 9 patients with single-site endometrioid ovarian and 26 patients with single-site endometrial endometrioid cancer. For all 64 patients, we performed sequencing of a 275-gene cancer panel combined with compartment-resolved mass spectrometry (MS) based proteomics of consecutive tissue sections to compare global (6,000+ proteins), tumor, and stromal proteomes. Results: DNA-based panel sequencing confirmed that most SEOCs are clonally related, suggesting primary and metastatic disease. These findings were further substantiated on the global proteome level, uncovering pronounced differences between SEOCs and single tumors and underscoring the importance of the stromal proteome in defining and identifying SEOCs. Our integrated proteogenomic approach confirmed that SEOCs more closely resemble endometrial endometrioid than endometrioid ovarian cancers. Conclusions: The integrated proteogenomic data show that SEOCs are distinguishable from endometrial endometrioid or endometrioid ovarian cancers. Based on their proteogenomic similarity to endometrial endometrioid cancers, we conclude that most synchronous endometrial and ovarian cancers represent primary endometrial endometrioid cancers that have metastasized to the ovary.

2025-03-11 | PXD059172 | Pride

Microsatellite stable (n=38) and instable-high (n=13) human colorectal tumors assayed with Affymetrix HuGeneFL arrays.

Project description:mRNA assays were performed on 51 samples of human colorectal tumors using Affymetrix HuGeneFL arrays containing 7129 probe-sets. We compared 38 microsatelite stable (MSS) tumors with 13 microsatellite instable-high (MSI) tumors to form a list of genes differing between the two types. In order to identify molecular signatures characterizing MSI tumors, we examined only MSI-high cancers and not MSI-low ones. Keywords: disease state analysis

2009-04-10 | GSE11543 | GEO

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