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EBF2 links KMT2D-mediated H3K4me1 to suppress pancreatic cancer progression via upregulating KLLN.

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE237366 | GEO | 2023/07/18

REPOSITORIES: GEO

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EBF2 links KMT2D-mediated H3K4me1 to suppress pancreatic cancer progression via upregulating KLLN [Cut&Tag]

Project description:CUT-Tag revealed a strong reduction of KMT2D, H3K4me1 and EBF2 signals at the transcription start site (TSS) and promoter regions of genes that were downregulated in KMT2D-depleted (KMT2D-KD) cells

2023-07-18 | GSE237365 | GEO

EBF2 links KMT2D-mediated H3K4me1 to suppress pancreatic cancer progression via upregulating KLLN [ChIP-seq]

Project description:ChIP-seq revealed a strong reduction of KMT2D, H3K4me1 and EBF2 signals at the transcription start site (TSS) and promoter regions of genes that were downregulated in KMT2D-depleted (KMT2D-KD) cells

2023-07-18 | GSE237364 | GEO

EBF2 links KMT2D-mediated H3K4me1 to suppress pancreatic cancer progression via upregulating KLLN [RNA-seq]

Project description:We sought to elucidate the roles of KMT2D- and EBF2-regulated H3K4me1 in gene expression through profiling the gene transcription in PDAC cells overexpressed with EBF2 (EBF2-OE) or activated by GSK-LSD1, a selective inhibitor of KDM1A/LSD1 which can increase H3K4me1 level via blocking the histone H3K4 demethylase activity of KDM1A/LSD1

2023-07-18 | GSE237363 | GEO

EBF2 links KMT2D-mediated H3K4me1 to suppress pancreatic cancer progression via upregulating KLLN.

Project description:EBF2 links KMT2D-mediated H3K4me1 to suppress pancreatic cancer progression via upregulating KLLN.

| PRJNA994823 | ENA

EBF2 links KMT2D-mediated H3K4me1 to suppress pancreatic cancer progression via upregulating KLLN [Cut&Tag]

Project description:EBF2 links KMT2D-mediated H3K4me1 to suppress pancreatic cancer progression via upregulating KLLN [Cut&Tag]

| PRJNA994830 | ENA

EBF2 links KMT2D-mediated H3K4me1 to suppress pancreatic cancer progression via upregulating KLLN [RNA-seq]

Project description:EBF2 links KMT2D-mediated H3K4me1 to suppress pancreatic cancer progression via upregulating KLLN [RNA-seq]

| PRJNA994828 | ENA

EBF2 links KMT2D-mediated H3K4me1 to suppress pancreatic cancer progression via upregulating KLLN [ChIP-seq]

Project description:EBF2 links KMT2D-mediated H3K4me1 to suppress pancreatic cancer progression via upregulating KLLN [ChIP-seq]

| PRJNA994829 | ENA

PRKRA promotes pancreatic cancer progression by upregulating MMP1 transcription via the NF-κB pathway.

Project description:ObjectivePancreatic cancer (PC) is highly malignant, but the underlying mechanisms of cancer progression remain unclear. PRKRA is involved in cellular stress response, but its role in PC was unknown.MethodsThe expression of PRKRA between normal and tumor tissues were compared, and the prognostic value of PRKRA was evaluated. SiRNA and plasmids were applied to investigate the effects of PRKRA on PC cells. Organoids and cell lines with knockout and overexpression of PRKRA were established by CRISPR/Cas9 and lentivirus. The effects of PRKRA on PC were evaluated in vivo by cell-derived xenografts. The downstream genes of PRKRA were screened by transcriptome sequencing. The regulation of the target gene was validated by RT-qPCR, western blot, ChIP and dual luciferase reporter assay. Besides, the correlation between PRKRA and gemcitabine sensitivity was investigated by PC organoids.ResultsPRKRA was significantly overexpressed in PC tissues and independently associated with poor prognosis. PRKRA promoted the proliferation, migration, and chemoresistance of PC cells. The proliferation of PC organoids was decreased by PRKRA knockout. The growth and chemoresistance of xenografts were increased by PRKRA overexpression. Mechanistically, PRKRA upregulated the transcription of MMP1 via NF-κB pathway. ChIP and dual luciferase reporter assay showed that NF-κB subunit P65 could bind to the promoter of MMP1. The sensitivity of PC organoids to gemcitabine was negatively correlated with the expression of PRKRA and MMP1.ConclusionsOur study indicated that the PRKRA/NF-κB/MMP1 axis promoted the progression of PC and may serve as a potential therapeutic target and prognosis marker.

| S-EPMC10361375 | biostudies-literature

KMT2D links TGF-β signaling to noncanonical activin pathway and regulates pancreatic cancer cell plasticity.

Project description:Although KMT2D, also known as MLL2, is known to play an essential role in development, differentiation, and tumor suppression, its role in pancreatic cancer development is not well understood. Here, we discovered a novel signaling axis mediated by KMT2D, which links TGF-β to the activin A pathway. We found that TGF-β upregulates a microRNA, miR-147b, which in turn leads to post-transcriptional silencing of KMT2D. Loss of KMT2D induces the expression and secretion of activin A, which activates a noncanonical p38 MAPK-mediated pathway to modulate cancer cell plasticity, promote a mesenchymal phenotype, and enhance tumor invasion and metastasis in mice. We observed a decreased KMT2D expression in human primary and metastatic pancreatic cancer. Furthermore, inhibition or knockdown of activin A reversed the protumoral role of KMT2D loss. These findings support a tumor-suppressive role of KMT2D in pancreatic cancer and identify miR-147b and activin A as novel therapeutic targets.

| S-EPMC10330100 | biostudies-literature

CSTF2T facilitates pancreatic adenocarcinoma growth and metastasis by elevating H3K4Me1 methylation of CALB2 via ASH2L.

Project description:Pancreatic adenocarcinoma (PAAD) is a major cause of mortality related to cancer worldwide. This paper dissected the functions of the CSTF2T/ASH2L/CALB2 axis in PAAD progression. CALB2 expression was assessed in PAAD tissues and cells using RT-qPCR and western blot. Subsequent to gain- and loss-of-function experiments in PAAD cells, cell apoptosis, invasion, proliferation, and migration were examined using flow cytometry, Transwell, CCK-8, and Scratch assays. Additionally, the expression of proliferation markers and apoptotic and metastasis- and invasion-related proteins was measured using western blot. The relationship among CALB2, KMT2D, ASH2L, H3K4Me1, and CSTF2T was evaluated using ChIP, RNA pull-down, RIP, and Co-IP assays. A nude mouse transplantation tumor model was established, with observation of tumor growth and metastasis. CALB2 expression was high in PAAD tissues and cells. Mechanistically, KMT2D was enriched in the CALB2 promoter, and CSTF2T bound to and upregulated ASH2L as a RNA binding protein, which was a core component of the KMT2D complex to enhance CALB2 expression through H3K4Me1 upregulation. CALB2 knockdown diminished the viability, invasion, and migration but elevated the apoptosis of PAAD cells. Likewise, CSTF2T knockdown suppressed the growth and metastasis of PAAD cells and transplanted tumors in nude mice, which was counteracted by further CALB2 overexpression. CSTF2T knockdown blocked the ASH2L/CALB2 axis to protect against PAAD growth and metastasis.

| S-EPMC10251778 | biostudies-literature

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