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CpG Hypermethylation and WNT/AP-1 cooperativity Define the Epigenetic Landscape and a Clinical Subgroup of High-Risk Pediatric Adrenocortical Carcinoma [methylation array]

ABSTRACT: Our integrative epigenomic analysis identified four molecularly distinct subgroups based on DNA methylation profiles, each marked by unique transcriptional programs, cellular compositions, and tissue architectures. These molecular subtypes outperformed traditional histopathological classifications in predicting clinical outcomes and addressed the longstanding lack of robust risk markers in pACT.

ORGANISM(S): Homo sapiens

PROVIDER: GSE308221 | GEO | 2026/08/12

REPOSITORIES: GEO

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CpG Hypermethylation and WNT/AP-1 cooperativity Define the Epigenetic Landscape and a Clinical Subgroup of High-Risk Pediatric Adrenocortical Carcinoma

Project description:Our integrative epigenomic analysis identified four molecularly distinct subgroups based on DNA methylation profiles, each marked by unique transcriptional programs, cellular compositions, and tissue architectures. These molecular subtypes outperformed traditional histopathological classifications in predicting clinical outcomes and addressed the longstanding lack of robust risk markers in pACT.

2026-08-12 | GSE343489 | GEO

CpG Hypermethylation and WNT/AP-1 cooperativity Define the Epigenetic Landscape and a Clinical Subgroup of High-Risk Pediatric Adrenocortical Carcinoma [Methylation array]

Project description:Treatment of three adult ACC cell lines (H295R and ACC1, ACC2) with entinostat and decitbaine led to consistent dose-dependent changes in DNA methylation patterns. These findings support entinostat's potential to reverse high-risk epigenetic programs in pACT and highlight HDAC inhibition as a promising therapeutic avenue, particularly when combined with established treatments.

2026-08-12 | GSE336709 | GEO

CpG Hypermethylation and WNT/AP-1 cooperativity Define the Epigenetic Landscape and a Clinical Subgroup of High-Risk Pediatric Adrenocortical Carcinoma [cell line]

Project description:Treatment of two adult ACC cell lines (H295R and CU-ACC1) with the HDAC inhibitor entinostat led to consistent dose-dependent reductions in viability, outperforming the DNA demethylating agent decitabine. scRNA-seq analyses revealed global transcriptional reprogramming. This included downregulation of AP-1 transcription factors (FOS, JUND, JUNB), suppression of oxidative phosphorylation and steroidogenic pathways, and increased expression of pro-apoptotic genes. These findings support entinostat's potential to reverse high-risk epigenetic programs in pACT and highlight HDAC inhibition as a promising therapeutic avenue, particularly when combined with established treatments.

2026-08-12 | GSE336546 | GEO

CpG Hypermethylation and WNT/AP-1 cooperativity Define the Epigenetic Landscape and a Clinical Subgroup of High-Risk Pediatric Adrenocortical Carcinoma [Visium HD]

Project description:To investiagte the cellular heterogenity one sample from each DNA methylation-based subgroup was investiagted using the Visium HD platform by 10x Genomics.

2026-08-01 | GSE316779 | GEO

Tumor DNA methylation profiling of pediatric patients with adrenocortical tumors

Project description:Abnormal DNA methylation contributes to tumor progression and is emerging as a prognostic marker in several types of cancers. To investigate whether DNA methylation is associated with Pediatric Adrenocortical Tumor (pACT) presentation and patient prognosis, we analyzed the methylation profile of 57 tumors (Illumina Infinium HumanMethylation850 BeadChip) and patients’ clinicopathological features and outcome.

2023-01-26 | GSE179175 | GEO

CpG Hypermethylation and WNT/AP-1 cooperativity Define the Epigenetic Landscape and a Clinical Subgroup of High-Risk Pediatric Adrenocortical Carcinoma

Project description:CpG Hypermethylation and WNT/AP-1 cooperativity Define the Epigenetic Landscape and a Clinical Subgroup of High-Risk Pediatric Adrenocortical Carcinoma

| PRJNA1511644 | ENA

PACT suppresses PKR activation through dsRNA binding and dimerization, and is a therapeutic target for triple-negative breast cancer

Project description:Triple-negative breast cancer (TNBC), the deadliest breast cancer subtype, lacks broadly applicable targeted therapies. Induction of ‘viral mimicry’ through activation of viral double-stranded RNA (dsRNA) sensors has potential therapeutic applications for TNBC and other cancers. Suppressors of dsRNA sensing prevent sensing of endogenous dsRNAs and resulting autoimmunity. Depletion of the suppressor of dsRNA sensing ADAR1 causes activation of dsRNA sensors and cell death in many cancer cell lines. These ADAR1-dependent cells are generally also dependent on the dsRNA-binding protein PACT, which is highly expressed and essential in many TNBC cell lines. While PACT is known as an activator of the dsRNA sensor PKR, overexpression of PACT had no effect on activation of PKR in multiple breast cancer cell lines. Conversely, depletion of PACT in PACT-dependent cell lines caused robust activation of the dsRNA sensor PKR and cell death, in addition to induction of integrated stress response genes and NF-κB targets. These phenotypes were entirely dependent on PKR. Rescue experiments revealed that PACT dimerization and dsRNA binding is required to suppress PKR activation. While depletion of PACT alone in ADAR1/ PACT-independent cell lines had no effect on PKR activation, combined depletion of both PACT and ADAR1 in those cell lines caused robust PKR activation and cell death, supporting a partially redundant role for ADAR1 and PACT in suppression of dsRNA sensing. Taken together, these findings support a vital role for PACT in suppression of PKR activation, and highlight the therapeutic potential of targeting PACT to treat TNBC.

2025-06-03 | GSE298233 | GEO

Effect of PACT knockout on LNCaP protate cancer cells

Project description:PACT, encoded by the PRKRA gene, is a double-stranded RNA binding protein which has two main mechanisms of action; functioning as an activator of both protein kinase RNA (PKR) and retinoic acid-inducible gene 1 (RIG-1) to facilitate innate antiviral defense mechanisms in mammals; and PACT is also an integral member of the cytoplasmic RNA-induced silencing complex (RISC) which enables the processing of pre-microRNAs into mature microRNAs (miRNAs). We previously described an alternate role for PACT as a nuclear receptor (NR) co-activator, which when recruited to hormone-regulated promoters can modulate the expression of NR-regulated genes. Here we employed a loss of function approach to investigate the role of PACT in prostate cancer (PCa). Depletion of PACT in human PCa cell lines resulted in a significant reduction in cell proliferation. RNA-sequencing analysis of LNCaP PCa cells ± PACT revealed that in the absence of PACT, various biological processes involved in proliferation were depleted, including cell cycle progression and division.

2025-12-02 | GSE253245 | GEO

Deletion of human tarbp2 reveals cellular microRNA targets and cell cycle function of TRBP

Project description:TRBP has two known functions as Dicer co-factor and PKR inhibitor. However, the role of TRBP in miRNA biogenesis is controversial and its regulation of PKR in mitosis remains unexplored. Here, we generate TRBP KO HeLa cells and find that TRBP depletion alters Dicer processing sites of a subset of miRNAs, but does not affect Dicer stability, miRNA abundance, or Argonaute loading. By generating PACT, another Dicer interactor, and TRBP/PACT double-KO cells, we further show that TRBP and PACT do not functionally compensate each other and that only TRBP contributes to Dicer processing. We also report that TRBP is hyperphosphorylated by JNK in M phase when PKR is activated by cellular dsRNAs. Hyperphosphorylation potentiates the inhibitory activity of TRBP on PKR, suppressing PKR in M-G1 transition. By generating the first human TRBP KO, our study clarifies the role of TRBP and unveils negative feedback regulation of PKR through TRBP phosphorylation. small RNAs of wild type, TRBP knockout, PACT knockout and TRBP/PACT double knockout cells were sequenced by Illumina Miseq.

2014-09-16 | E-GEOD-61458 | biostudies-arrayexpress

CpG Hypermethylation and WNT/AP-1 cooperativity Define the Epigenetic Landscape and a Clinical Subgroup of High-Risk Pediatric Adrenocortical Carcinoma [Visium HD]

Project description:CpG Hypermethylation and WNT/AP-1 cooperativity Define the Epigenetic Landscape and a Clinical Subgroup of High-Risk Pediatric Adrenocortical Carcinoma [Visium HD]

| PRJNA1404185 | ENA

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