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Downstream genes and pathways of ASH1-miR-375-YWHAZ axis in hepatocellular carcinoma

ABSTRACT: To explore the mechanism and downstream pathways of ASH1-miR-375-YWHAZ axis in hepatocellular carcinoma (HCC). We performed microarray assay to identify the downstream genes of YWHAZ. As a result, we obtained 507 (245 upregulation and 262 downregulation) differentially expressed genes significantly affected by YWHAZ knockdown. Function enrichment analysis showed that these genes were enriched in the “Regulation of actin cytoskeleton” pathway which is related with cell migration and tumor metastasis. We also find that most of the autophagy-associated genes, such as ATG3, ATG5 and ATG7 and EMT related gene E-cadherin were highly correlated with YWHAZ and changed by silencing YWHAZ. Real-time quantitative RT-PCR was performed to verify the microarray results. In conclusion, the expression profile of many genes were significantly affected by YWHAZ knockdown, which helps to further explore the mechanism of the effects of ASH1-miR-375-YWHAZ axis in HCC.

ORGANISM(S): Homo sapiens

PROVIDER: GSE98026 | GEO | 2022/10/05

REPOSITORIES: GEO

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Homo sapiens

Project description:Downstream genes and pathways of ASH1-miR-375-YWHAZ axis in hepatocellular carcinoma

| PRJNA383713 | ENA

The ASH1-miR-375-YWHAZ Signaling Axis Regulates Tumor Properties in Hepatocellular Carcinoma.

Project description:Hepatocellular carcinoma (HCC) is a worldwide malignance, and the underlying mechanisms of this disease are not fully elucidated. In this study, the existence and function of achaete-scute homolog-1 (ASH1)-miR-375-YWHAZ signaling axis in HCC were determined. Our experiments and the Cancer Genome Atlas (TCGA) sequencing data analyses showed that ASH1 and miR-375 were significantly downregulated, whereas YWHAZ was significantly upregulated in HCC. Furthermore, we found that ASH1 positively regulates miR-375, and miR-375 directly downregulates its target YWHAZ. Gain- and loss-of-function study demonstrated ASH1 and miR-375 function as tumor suppressors, whereas YWHAZ acts as an oncogene in HCC. Animal experiment indicated that YWHAZ small interfering RNAs (siRNAs) (si-YWHAZ) delivered by nanoliposomes could suppress the growth of hepatoma xenografts and was well tolerant by nude mice. Further studies revealed that YWHAZ was involved in several protein networks, such as cell autophagy, epithelial-mesenchymal transition (EMT), apoptosis, cell cycle, invasion, and migration. In addition, the patient group with ASH1-high-expression-miR-375-high-expression-YWHAZ-low-expression was correlated with a better clinical prognosis compared with the opposite expression group. In conclusion, we proved the existence of ASH1-miR-375-YWHAZ signaling axis and interpreted its important role in driving HCC tumor progression.

| S-EPMC5944419 | biostudies-literature

YWHAZ is an Invasion and Metastasis promoting genes of Lung cancer

Project description:Metastasis is a major cause leading to mortality for lung cancer patients. We identified YWHAZ as a potential metastasis-promoting candidate and found that overexpression of YWHAZ promotes lung cancer cell proliferation, anchorage-independent growth, migration, and invasion in vitro, as well as tumorigenesis and metastasis in vivo. It not only increases cell protrusions and branchings but also induces epithelial-mesenchymal transition. Most importantly, YWHAZ protein could prevent Â£]-catenin from ubiquitination via its association with Â£]-catenin and enhance slug transcriptional activity which is regulated by Â£]-catenin/TCF signaling pathway. Moreover, YWHAZ expression was higher in tumors than in adjacent normal tissues in 63 Non-small-cell lung cancer (NSCLC) patients. NSCLC patients with high YWHAZ expressing tumors had shorter overall survival than those with low-expressing tumors. We conclude that YWHAZ play a critical role in promoting NSCLC metastasis. In this investigation, we used a lung cancer invasion cell model to identify the genes involved in cancer progression. YWHAZ is a potential oncogene whose expression is correlated to the survival of patients with breast, prostate and liver cancers. However, the role of YWHAZ in lung caner progression has not been reported, particularly in metastasis. Here, YWHAZ was ectopically expressed in lower invasive lung cancer cell line its impact on colonogenesis, migration and invasiveness was assessed. The underlying mechanism was explored by YWHAZ-expressed transfectants and microarrays and the clinical relevance was evaluated by quantitative RT-PCR.

2012-11-07 | E-GEOD-20318 | biostudies-arrayexpress

RNA-sequencing from miR-375 knockout and YAP overexpression lung carcinoid (H727) cells.

Project description:We report RNA sequencing data for miR-375 knockout and YAP overexpression lung carcinoid cells (H727). Lung carcinoids are variably aggressive and mechanistically understudied neuroendocrine neoplasms (NENs). Here, we identified and elucidated the function of a miR-375/yes-associated protein (YAP) axis in lung carcinoid (H727) cells. miR-375 and YAP are respectively high and low expressed in wild-type H727 cells. Following lentiviral CRISPR/Cas9-mediated miR-375 depletion, we identified distinct transcriptomic changes including dramatic YAP upregulation. Similarly, YAP overexpression resulted in distinct and partially overlapping transcriptomic changes, phenocopying the effects of miR-375 depletion in the same models as above. Pathways analysis and confirmatory real-time PCR studies of shared dysregulated targets indicate that this axis controls neuroendocrine related functions such as neural differentiation, exocytosis, and secretion. Taken together, we provide compelling evidence that a miR-375/YAP axis is a critical mediator of neuroendocrine differentiation and tumorigenesis in lung carcinoid cells.

2021-05-19 | GSE154872 | GEO

Mrg15 allosterically activates Ash1’s H3K36 methyltransferase activity and facilitates Ash1’s trithorax group protein function in Drosophila

Project description:Ash1 is a classic Trithorax group protein possessing an H3K36-specific histone methyltransferase activity. Ash1 plays a critical role in antagonizing Polycomb silencing and its loss-of-function mutations lead to inactivation of certain Hox genes and homeotic transformation. Here, we report the purification of Ash1 complex with the identification of two novel subunits, Mrg15 and Nurf55. Interestingly, Mrg15 stimulates the enzymatic activity of Ash1 in vitro, and such stimulation is independent of the chromo domain of Mrg15. In vivo, Mrg15 is recruited by Ash1 to their common target genes and Mrg15 is essential for the proper deposition of H3K36me2 at these regions.

2017-10-04 | GSE93100 | GEO

YWHAZ is an Invasion and Metastasis promoting genes of Lung cancer

2012-11-07 | GSE20318 | GEO

Pre-miR-375_A549 vs. Pre-miR-NC#2 (Ambion) _A549

Project description:We investigated the functional significance of ASH1-inducible miR-375 in terms of biologic phenotypes of ASH1-positive lung cancer cells. To this end, we conducted genome-wide expression profiling analysis of miR-375-transfected A549 cells. Microarray analysis using a Whole Human Genome 4 x 44K Microarray G4112F (Agilent) was conducted to examine changes in expression of potential target genes of miR-375 by transfection of Pre-miR-375 or Pre-miR-NC#2 (Ambion) in A549 cells, which were then harvested at 12, 24, 48, and 96 hours after transfection.

2011-10-31 | E-GEOD-31566 | biostudies-arrayexpress

Pre-miR-375_A549 vs. Pre-miR-NC#2 (Ambion) _A549

2011-10-31 | GSE31566 | GEO

Trithorax-group protein ASH1 defines novel H3K36me3/H3K9me3 bivalent domains

Project description:A Trithorax-group (TrxG) protein ASH1 selectively dimethylates histone H3 lysine 36 (H3K36) and is required for expression of Hox genes. Genome-wide targets and molecular functions of ASH1, however, have remained elusive. Here we report ChIP-seq analysis of ASH1 targets in the human genome using a leukemia cell line K562. We identified 4,596 ASH1 binding sites, 2,502 of which are in the coding region, mostly in a proximity of promoters. Remaining half of the ASH1 binding sites are in the intergenic region. Analysis of histone methyation patterns revealed that a majority of ASH1 bidning sites are closely associated not only with trimethylated H3K36 (H3K36me3) but also with H3K9me3, shedding light for the first time to H3K36/H3K9 double methylation domains. Of note, an H3K9 methyltransferase SETDB1 is enriched in the ASH1 bidning sites, whereas EZH2 but not SUZ12 of the Polycomb Repression Complex 2 (PRC2) is present in bivalent domains. In addition, a small subset of ASH1 targets bear H3K4me3 and colocalize with RNA polymerase II. These select targets are highly enriched for regulators of gene expression, such as CXXC1, WHSC2/NELFA, and a battery of zinc finger proteins, suggesting that ASH1 might acts as a master regulator of gene expression.

2016-12-28 | GSE76145 | GEO

ASH1 Q4177.S2

Project description:modENCODE_submission_2984 This submission comes from a modENCODE project of Gary Karpen. For full list of modENCODE projects, see http://www.genome.gov/26524648 Project Goal: We aim to determine the locations of 125 chromosomal proteins across For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf EXPERIMENT TYPE: CHIP-chip. BIOLOGICAL SOURCE: Cell Line: S2-DRSC; Tissue: embryo-derived cell-line; Developmental Stage: late embryonic stage; Sex: Male; NUMBER OF REPLICATES: 4; EXPERIMENTAL FACTORS: Cell Line S2-DRSC; Antibody ASH1 Q4177 (target is ASH1)

2010-11-18 | E-GEOD-25361 | biostudies-arrayexpress

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