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ANP32B promotes colorectal cancer cell progression and reduces cell sensitivity to PRAP1 inhibitor through up-regulating HPF1

ABSTRACT: The aim of this work is to explore the role of ANP32B on CRC development

ORGANISM(S): Homo sapiens

PROVIDER: GSE247230 | GEO | 2023/11/24

REPOSITORIES: GEO

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ANP32B promotes colorectal cancer cell progression and reduces cell sensitivity to PRAP1 inhibitor through up-regulating HPF1

Project description:ANP32B promotes colorectal cancer cell progression and reduces cell sensitivity to PRAP1 inhibitor through up-regulating HPF1

| PRJNA1036664 | ENA

ANP32B-mediated repression of p53 contributes to maintenance of normal and CML stem cells

Project description:we demonstrate that conditional deletion of acidic leucine-rich nuclear phosphoprotein 32B (ANP32B) in hematopoietic cells impairs repopulation capacity and postinjury regeneration of HSCs. Mechanistically, ANP32B forms a repressive complex with and thus inhibits the transcriptional activity of p53 in hematopoietic cells, and p53 deletion rescues the functional defect in Anp32b-deficient HSCs. Of great interest, ANP32B is highly expressed in leukemic cells from patients with chronic myelogenous leukemia (CML). Anp32b deletion enhances p53 transcriptional activity to impair LSC function in a murine CML model and exhibits synergistic therapeutic effects with tyrosine kinase inhibitors in inhibiting CML propagation. In summary, our findings provide a novel strategy to enhance p53 activity in LSCs by inhibiting ANP32B and identify ANP32B as a potential therapeutic target in treating CML.

2021-09-27 | GSE184474 | GEO

LYAR promotes colorectal cancer progression by up-regulating FSCN1 expression and fatty acid metabolism

Project description:Colorectal cancer (CRC) is a highly malignant tumor associated with poor prognosis, yet the molecular mechanisms are not fully understood. In this study, we showed that LYAR, a nucleolar protein, expresses at a higher level in CRC than adjacent normal tissue and LYAR expression is closely associated with distant CRC metastasis. LYAR not only significantly promotes the migration and invasion of CRC cells in vitro, also the knockdown (KD) of LYAR in CRC cells inhibits xenograft tumor metastasis in vivo. Microarray analysis of LYAR KD cells combined with ChIP assay, gene reporter assay and rescue experiment indicate that FSCN1 (encoding fascin actin-bundling protein 1, Fascin-1) serves as a new key regulator of the LYAR-promoted migration and invasion of CRC cells. Knockdown of FSCN1 significantly inhibits subcutaneous tumorigenesis of CRC cells, and leads to the down-regulation of FASN and SCD, genes encoding key enzymes in fatty acid synthesis. In summary, this study reveals a novel mechanism by which LYAR promotes tumor cell migration and invasion by up-regulating FSCN1 expression and affecting fatty acid metabolism in CRC.

2021-07-17 | GSE180263 | GEO

The histone chaperone ANP32B regulates chromatin incorporation of the atypical human histone variant macroH2A

Project description:Eukaryotic chromatin structure is highly conserved, with the canonical histone proteins revealing only small sequence changes across species. Yet, all vertebrates exhibit three much larger histone H2A variants, macroH2A. A distinctive feature of these atypical histones is the globular macrodomain module, which can bind metabolites and is connected to the histone fold through a flexible linker. MacroH2A variants impact heterochromatin organization, transcription regulation and establish a barrier for cellular reprogramming. However, the mechanisms of how these large H2A variants are incorporated into chromatin and the identity of any chaperones required for histone deposition have remained elusive. Here, we developed a split-GFP-based cellular readout for histone incorporation and conducted a genome-wide mutagenesis screen in haploid human cells to identify proteins that regulate macroH2A dynamics. We identified and validated the histone chaperone ANP32B as a regulator of macroH2A chromatin deposition. ANP32B associates with macroH2A in cells and in vitro binds to histones with low nanomolar affinity. In vitro nucleosome assembly assays show that ANP32B stimulates deposition of macroH2A-H2B and not of H2A-H2B onto tetraso me. In cells, depletion of ANP32B in cells strongly affects global macroH2A deposition, revealing ANP32B as a macroH2A chaperone. Our study highlights the power of haploid cell functional genomics coupled with cellular imaging to identify factors that are required for chromatin plasticity and diversity.

2023-11-07 | GSE241387 | GEO

RNA-seq for MV4-11 cell line in either the absence or presence of ANP32B

Project description:Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are to compare RNA-seq results for MV4-11 cell line in either the absence or presence of ANP32B

2023-09-12 | GSE242849 | GEO

RNA-seq for Kasumi-1 cell line in either the absence or presence of ANP32B

Project description:Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are to compare RNA-seq results for Kasumi-1 cell line in either the absence or presence of ANP32B

2023-09-12 | GSE242848 | GEO

LYAR promotes colorectal cancer progression by up-regulating FSCN1 expression and is closely related to fatty acid metabolism

Project description:Colorectal cancer (CRC) is a highly malignant tumor associated with a poor prognosis, yet the molecular mechanisms are not fully understood. In this study, we showed that LYAR expresses at a higher level in CRC than normal tissue and LYAR expression is closely associated with distant CRC metastasis. LYAR significantly promotes the migration and invasion of CRC cells in vitro, and reduction of LYAR expression in CRC cells inhibites xenograft tumor metastasis in vivo. Microarray analysis of LYAR knockdown (KD) cells combined with ChIP assay, gene reporter assay and rescue experiment indicate that FSCN1 (fascin actin-bundling protein 1, Fascin-1) serves as a new and key regulator of the LYAR-promoted migration and invasion of CRC cells. In addition, knockdown of FSCN1 significantly inhibites subcutaneous tumorigenesis of CRC cells. Moreover, we found that FSCN1 affects some key enzymes in lipid fatty acid metabolism such as FASN and SCD. In summary, this study reveals a novel mechanism by which LYAR promotes tumor cell migration and invasion by up-regulating FSCN1 expression and further promoting fatty acid synthesis in CRC.

2021-07-26 | GSE180805 | GEO

Cell lines with either no treatment or ANP32B knockdown

Project description:Cell lines with either no treatment or ANP32B knockdown

| PRJNA1015158 | ENA

A novel USP4 inhibitor suppresses colorectal cancer stemness and enhances chemotherapy sensitivity by promoting the degradation of β-catenin and Twist1

Project description:The high mortality rate of metastasis colorectal cancer (CRC) is mainly due to chemotherapy resistance. Evidence implicates cancer stem cells (CSCs) play essential roles in chemoresistance. The deubiquitinating enzymes are vital regulators in both CSCs maintenance. Targeting deubiquitinase might be potential strategies to clear CSCs and overcome chemotherapy resistance. Here, we demonstrated that ubiquitin-specific peptidase 4 (USP4) is a key regulator of cancer stemness by stabilizing β-catenin and Twist1 proteins in CRC cells. Additionally, U4-I05, a novel natural small molecule that targets the enzyme activity of USP4 is characterized. U4-I05 binds to the catalytic domain of USP4 at nanomolar concentrations, resulting in the proteasome-mediated degradation of β-catenin and Twist1. Furthermore, U4-I05 attenuated CSC features and augmented sensitivity to oxaliplatin and 5-fluorouracil. In a genetically engineered CRC mouse model, U4-I05 inhibited tumor metastasis and prolonged survival. Overall, this study identifies U4-I05 as a USP4 inhibitor that has meaningful efficacy toward CRC.

2025-01-29 | GSE272835 | GEO

Resistance to PI3K/mTOR inhibitor PF-04691502 in KRAS mutant colorectal cancer models reveals a sensitivity to combination with EGFR inhibition

Project description:We explored potential bypass mechanisms to PI3K/mTOR-directed therapy in KRAS mutant CRC models, utilizing genetically engineered mouse models (GEMM) to generate acquired resistance to the targeted dual PI3K/mTOR small molecule inhibitor PF-04691502. Transcriptomic analysis revealed a dynamic stem-like progenitor signature which was increased in the presence of drug pressure.

2014-08-31 | E-MTAB-2510 | biostudies-arrayexpress

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