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Dynamic interaction of MYC enhancer RNA with YEATS2 protein regulates MYC gene transcription in pancreatic cancer.

EMBO Rep · 2025
90/100 3/4
Why this verdict

The main results reproduced: recomputed values matched the published ones within tolerance.

Reproduced on the brainbox compute brainarbeit.com
How its reproducibility compares
90/100
Reproducibility score
0.9 SD above mean
vs. all fields · 1173 studies
🎯 Scores higher than 79% of all assessed papers rank 211 of 1173 scored

A 0–100 reproducibility-quality score from the per-question grades, shown as a z-score: standard deviations above (+) or below (−) the mean of comparable assessments.

Reproduction agent’s raw note

Described well enough to reproduce 1:1. Fresh, independent re-run from raw GSE288088 FASTQ on «our HPC» SLURM («job», 2026-06-23) of the fully-specified pipeline: FastQC 0.11.7 -> Trim Galore 0.6.10 -> Bowtie2 (default, hg38 GRCh38_noalt_as, unique reads) -> HOMER makeTagDirectory/findPeaks -style groseq/coverage. C1 (headline eRNA count) is an EXACT integer match: 19 eRNAs in the 260 kb MYC super-enhancer (chr8:127,163,754-127,428,551) at both per-condition pools, matching the paper. C2 (TNFa induction, Fig 1B) reproduces qualitatively at all 4 loci (24h>0h). V (validation) shows strong matched-strand concordance (|r|=0.89-0.99) with the authors' deposited BigWigs. Alignment rates (96.04/95.97/96.00/95.69%) and unique-read counts are identical to an earlier 2026-06-20 run, confirming the pipeline is deterministic; that earlier genuine run had been lost to a false-positive infrastructure quarantine (its «infra» workdir reclaimed). NOT attempted: external overlay ChIP/ATAC datasets (out of scope) and all wet-lab/experimental results (not pipeline-derived). Grades are provisional and must be human-checked.

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Assessment versions

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  1. v1 current initial assessment Score 90
    assessed: 2026-06-20 ⛓ 2e06c8a79def
✎ I am an author of this paper

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Reproduced
2026-06-23
Rubric version
not recorded
Assessed by
Last updated
2026-08-05

Provisional, curator- or AI-assessed, and independently checkable. A reproduction outcome states what one attempt could reproduce — not a judgement of the authors.

Deep full-text extraction

Model: sonnet
Founding hypothesis

The paper tests whether a MYC-associated enhancer RNA (eRNA), induced under chronic inflammatory (TNF-α) conditions, regulates MYC gene transcription in pancreatic cancer cells through interaction with the histone reader protein YEATS2.

Core claims
  • MYC eRNAs (notably MYC-490-kb) are transcribed from the MYC super-enhancer and are upregulated by chronic TNF-α stimulation specifically in pancreatic cancer cells, not normal pancreatic epithelial cells finding
  • MYC-490-kb eRNA levels are elevated in chronic pancreatitis patient samples and in pancreatic cancer tissue versus adjacent normal tissue finding
  • MYC-490-kb eRNA positively regulates MYC mRNA transcription (knockdown reduces, overexpression increases MYC mRNA) in a dose-dependent manner finding
  • MYC-490-kb eRNA interacts with YEATS2 protein in a TNF-α-dependent, cancer-cell-specific manner finding
  • YEATS2 is required for MYC gene transcription, as its knockdown reduces MYC mRNA levels finding
  • TNF-α induces tyrosine dephosphorylation of the YEATS domain (involving residue Y313), which increases MYC eRNA binding to YEATS2 mechanism
  • MYC gene amplification is associated with reduced overall survival in PDAC patients (TCGA PAAD cohort) finding
  • MYC eRNA augments recruitment of the YEATS2-containing ATAC-HAT complex to the MYC promoter/enhancer, driving MYC expression mechanism
Experimental setups
Assay System Perturbation Readout Platform
Survival analysis (TCGA PAAD cohort) PDAC patient cohort, n=176 none (MYC amplification status) overall survival TCGA database
ChIP-seq (H3K27ac, H3K4me1) and ATAC-seq PDAC cell line (published datasets) none active enhancer marks / open chromatin at MYC super-enhancer
Nascent RNA sequencing MIAPaCa-2 cells TNF-α (24h) enhancer-directed transcription/eRNA levels from MYC super-enhancer
RT-PCR/qPCR MIAPaCa-2, AsPC-1, HPNE (and HCT-116) cells TNF-α (24h) MYC-490-kb, MYC-425-kb eRNA and MYC mRNA levels
qPCR on patient samples Chronic pancreatitis patients (n=7) and pancreatic cancer patient tissue (n=5) vs normal/adjacent normal none (disease state) MYC-490-kb eRNA and MYC mRNA levels
Click-iT nascent RNA capture with nuclear/cytosolic fractionation MIAPaCa-2 and HPNE cells TNF-α subcellular localization of nascent MYC-490 eRNA Click-iT kit; Western blot (β-Actin, Lamin)
shRNA knockdown MIAPaCa-2 cells (MYC-490-kb eRNA KD and YEATS2 KD) shRNA knockdown MYC mRNA/eRNA and YEATS2 levels
Plasmid overexpression MIAPaCa-2 and HPNE cells MYC-490-kb / MYC-425-kb eRNA overexpression (dose titration) MYC mRNA levels
In-silico RNA-protein interaction prediction MYC-490-kb eRNA vs histone modifier proteins none binding propensity/docking score RPIseq, HDOCK web server
UV-RIP (RNA immunoprecipitation) MIAPaCa-2, AsPC-1, HPNE cells TNF-α stimulation YEATS2-associated MYC-490 eRNA (and BRD4 association)
Western blot / immunoprecipitation (phospho-tyrosine, 4G10 antibody) MIAPaCa-2, AsPC-1, HPNE cells; HEK293T-expressed YEATS domain, Y313/Y313F mutants TNF-α; in vitro phosphatase assay tyrosine phosphorylation of YEATS2/YEATS domain and correlation with eRNA binding
Key results
  • MYC-amplified PDAC patients show significantly lower overall survival than unaltered patients P=0.018, n=176
  • MYC-490-kb and MYC-425-kb eRNA and MYC mRNA levels increase after TNF-α treatment in MIAPaCa-2 and AsPC-1 cells but not HPNE P=0.0068/0.0419/0.0483 (MIAPaCa-2); P=0.0005/0.0015/0.0008 (AsPC-1)
  • MYC-490-kb eRNA is elevated in chronic pancreatitis patient samples vs normal P=0.0167, n=7 vs 7
  • MYC-490-kb eRNA and MYC mRNA are upregulated in pancreatic cancer tissue compared to adjacent normal tissue n=5
  • shRNA knockdown of MYC-490-kb eRNA reduces MYC mRNA expression ~30% reduction
  • Overexpression of MYC-490-kb eRNA (peaking at 200 ng DNA) significantly increases MYC mRNA in MIAPaCa-2 cells but not HPNE cells P=0.0025 (upper), P=0.0051 (lower panel)
  • UV-RIP shows increased YEATS2-MYC-490-kb eRNA association under TNF-α in MIAPaCa-2 and AsPC-1, but not HPNE; no increase seen with BRD4 or MYC-425-kb eRNA P=0.0001/0.0002 (MIAPaCa-2); P=0.0012/0.002 (AsPC-1)
  • shRNA knockdown of YEATS2 significantly reduces cMYC mRNA expression P=0.0017 to <0.0001 across 4 shRNAs
Key statistics
  • pvalue P=0.018 (survival difference by MYC amplification status, TCGA PAAD)
  • pvalue P=0.0068, P=0.0419, P=0.0483 (MYC-490, MYC-425 eRNA and MYC mRNA induction by TNF-α in MIAPaCa-2)
  • pvalue P=0.0005, P=0.0015, P=0.0008 (MYC-490, MYC-425 eRNA and MYC mRNA induction by TNF-α in AsPC-1)
  • pvalue P=0.0167 (MYC-490-kb eRNA elevated in chronic pancreatitis patients vs normal)
  • fold_change ~30% reduction (MYC mRNA decrease after MYC-490-kb eRNA knockdown)
  • count n=5 (pancreatic cancer patient tissue samples vs adjacent normal analyzed for MYC-490 eRNA/mRNA)
  • pvalue P=0.0001 (Input), P=0.0002 (IP) (UV-RIP YEATS2-MYC-490 eRNA association in TNF-treated MIAPaCa-2)
  • pvalue P=0.0026 (Input), P=0.027 (IP) (in vitro MYC eRNA binding assay correlating tyrosine dephosphorylation with YEATS domain binding)

Statistical methods review

Model: sonnet

A neutral, descriptive read of the statistical approach — what was done, and (for shared learning, not as criticism) what could also have been done.

The study combined TCGA public cohort survival analysis (n=176), in vitro cell-line assays in two pancreatic cancer lines and one normal epithelial line, and patient tissue comparisons (chronic pancreatitis n=7/group; pancreatic cancer n=5 vs. adjacent normal). Primary statistical inference across all quantitative assays (RT-PCR/qPCR) relied on repeated application of unpaired two-tailed Student's t-tests on n=3 independent experiments. Results were reported as mean ± SD with exact p-values; no multiplicity correction was described.

Replicationbiological Sample sizen=3 independent experiments for all cell-line assays; n=7 per group (chronic pancreatitis vs. normal); n=5 patients with matched adjacent normal tissue; n=176 TCGA PAAD patients for survival analysis GroupsTNF-α-treated vs. untreated cancer cell lines; cancer cell lines vs. normal epithelial cell line (HPNE); chronic pancreatitis patients vs. healthy controls; pancreatic tumor vs. adjacent normal tissue; MYC-amplified vs. MYC-unaltered TCGA PAAD patients Pairingmixed Randomization/blindingnot stated DispersionSD Exact p-valuesyes Effect sizesno Confidence intervalsno Multiplicity correctionnone stated
Statistical tests used
Test Applied to n Assumptions
Survival analysis — test not explicitly named (log-rank is the standard method for this output type) Fig 1A — overall survival by MYC amplification status in TCGA PAAD cohort 176 patients not stated
Unpaired two-tailed Student's t-test Fig 1C–E — RT-PCR of MYC eRNA and MYC mRNA in MIAPaCa-2, AsPC-1, HPNE at TNF-α 0 h vs 24 h n=3 independent experiments per cell line not stated
Unpaired two-tailed Student's t-test Fig 1F — MYC-490-kb eRNA in chronic pancreatitis vs. normal patient samples n=7 normal, n=7 chronic pancreatitis patients not stated
Unpaired two-tailed Student's t-test (as inferred from study-wide pattern; pairing not stated) Fig 1G — MYC-490-kb eRNA and MYC mRNA in pancreatic cancer vs. adjacent normal tissue n=5 patients not stated
Unpaired two-tailed Student's t-test Figs 2A–D — Click-iT nascent RNA fractionation, shRNA knockdown, eRNA overexpression in MIAPaCa-2 and HPNE n=3 independent experiments not stated
Unpaired two-tailed Student's t-test Figs 3A–B, 3E, 3J, 3L — UV-RIP quantification, YEATS2 KD effect on cMYC, in vitro eRNA binding with phospho-mutants n=3 independent experiments not stated
Approaches that could also have been used
  • Numerous unpaired t-tests were applied across multiple figures, cell lines, and shRNA constructs without any correction for multiple comparisons
    Could also: One-way or two-way ANOVA (depending on factorial structure) followed by a post-hoc test such as Tukey HSD or Dunnett's vs. control, or application of Benjamini-Hochberg FDR correction across the full set of t-tests — When many pairwise tests are performed, an omnibus test or explicit correction controls the family-wise error rate and reduces the probability of spurious findings accumulating across the experiment set
  • Pancreatic cancer tissue (n=5) was compared to matched adjacent normal tissue from the same patients using an unpaired test framework
    Could also: A paired t-test, or Wilcoxon signed-rank test given the very small n, that treats each patient's tumor/normal pair as a matched unit — Paired analysis removes between-patient variability and typically increases statistical power, more accurately reflecting the within-patient contrast between tumor and normal tissue
  • Parametric unpaired t-tests were applied to cell-line data from n=3 independent experiments
    Could also: Non-parametric Mann-Whitney U test, or supplementing bar graphs with plots of individual data points — With n=3, normality cannot be formally assessed; non-parametric alternatives require no distributional assumption, and displaying individual data points alongside summary statistics preserves the full distribution for readers
  • The survival analysis (Fig 1A) reports P=0.018 but does not name the underlying statistical test
    Could also: Explicitly state the log-rank test and report a hazard ratio with 95% confidence interval — Naming the test and providing a hazard ratio with CI conveys both the analytical basis and the magnitude and precision of the survival difference, improving interpretability and reproducibility
  • Effect magnitude was conveyed only through p-values and visual inspection of bar chart heights
    Could also: Report standardized effect sizes (e.g., Cohen's d) or fold changes with 95% confidence intervals alongside p-values — Effect size metrics separate statistical significance from biological magnitude, helping readers assess practical relevance and enabling future meta-analyses or power calculations
  • Dispersion was reported as SD across all quantitative figures with n=3
    Could also: Report 95% confidence intervals or show individual data points, approaches increasingly recommended for small-n experimental data — For n=3, the SD describes sample spread but CIs communicate precision of the mean estimate; individual data points additionally reveal the actual distribution and any outliers, consistent with current reporting standards in molecular biology journals
Software: RPIseq (in silico RNA-protein interaction prediction) · HDOCK web server (in silico docking) · UCSC Genome Browser (visualization of sequencing tracks) · Statistical software for t-tests (not named)

What was reproduced

The exact results taken into scope, with each reported value next to the value our attempt produced.

Scope — pmid-40216980

Paper: Roy et al. 2025, EMBO Rep — "Dynamic interaction of MYC enhancer RNA with YEATS2 protein regulates MYC gene transcription in pancreatic cancer." DOI 10.1038/s44319-025-00446-0 · PMCID PMC12117045.

Data: GEO GSE288088 (BioProject PRJNA1216178) — ex vivo Nascent RNA-seq (5-EU Click-iT capture, nuclear fraction) of MIA PaCa-2 cells, TNFα 0 h vs 24 h, 2 biological replicates each. 4 paired-end (2×100 bp) NovaSeq 6000 runs:

  • SRR32136284 → GSM8758825 — 0 h rep1 (~42.0 M spots)
  • SRR32136283 → GSM8758826 — 0 h rep2 (~47.2 M spots)
  • SRR32136282 → GSM8758827 — 24 h rep1 (~33.9 M spots)
  • SRR32136281 → GSM8758828 — 24 h rep2 (~36.0 M spots) Deposited processed data = strand-specific BigWig coverage tracks (rep1 only): 0hneg/0hpos (GSM8758825), 24hneg/24hpos (GSM8758827).

Code link in record: github.com/FelixKrueger/TrimGalore (Trim Galore v0.6.10, tag commit 4edff97). This is a third-party tool, not author code — valid per brief rule P16. The full pipeline is third-party tools chained per the Methods.

Pipeline (fully specified in Methods "Bioinformatic processing" + GEO data_processing)

  1. FastQC v0.11.7 — QC of raw reads.
  2. Trim Galore v0.6.10 — adapter trimming.
  3. Bowtie2 (Langmead & Salzberg 2012), default parameters, align to hg38; retain only uniquely aligned reads.
  4. HOMER makeTagDirectory from uniquely-aligned SAM/BAM.
  5. HOMER findPeaks -style groseq — call nascent transcripts (eRNAs).
  6. HOMER makeBigWig.pl -strand — strand-specific coverage BigWigs (UCSC viz).

IN SCOPE (pipeline-derived, attempted)

  • C1 — transcript/eRNA call. "MYC-490-kb and MYC-425-kb eRNA are part of a group of 19 eRNAs expressed from a 260 kb region (chr8:127,163,754–127,428,551) of the MYC super-enhancer" (Results, ¶ "MYC eRNAs are expressed from super-enhancer regions"). → reproduce by HOMER findPeaks -style groseq, count transcripts in that interval. PRIMARY pinnable claim.
  • C2 — TNFα induction (Fig 1B). Nascent RNA-seq signal at MYC-490 / MYC-425 eRNA and MYC loci is higher at 24 h than 0 h TNFα. → quantify coverage over the SE region / MYC gene, 0 h vs 24 h; check direction (increase).
  • V — track concordance. Correlate our reproduced strand BigWigs vs the authors' deposited BigWigs over the MYC locus (chr8:127–128 Mb). Validates the alignment step independent of the claim text.

OUT OF SCOPE (not attempted — reason)

  • ChIP-seq/ATAC-seq re-analysis of external datasets (GSE64557 H3K27ac/H3K4me1, GSE164974 ATAC) shown as overlay tracks in Fig 1B — external data, supportive context, not the GSE288088 result; HOMER -style histone/-style dnase runs are optional 20%. Could be added; skipped under 80/20.
  • All wet-lab / qPCR / RT-PCR / UV-RIP / Co-IP / ChIP-qPCR / phosphatase / MTT / wound-healing / survival / in-silico docking (RPISeq/HDOCK) results (Figs 1C–G, 2–5, EV1–4) — manual/experimental, not pipeline-derived.

Heavy compute

All alignment/HOMER runs on «our HPC» SLURM (account=kubisch_std, partition=std). Data + index + intermediates on «infra»; only small derived values returned to «host».

Figures / tables: Fig 1B
C1_eRNA_count_MYC_SE
Reported
19 eRNAs in chr8:127,163,754-127,428,551 (260 kb MYC super-enhancer)
Reproduced
19 transcripts in that interval (pool_0h=19, pool_24h=19; pooled-all=20)
exact
C2_TNFa_induction
Reported
nascent signal at MYC-490/MYC-425 eRNA & MYC gene higher at 24h vs 0h TNFa (Fig 1B)
Reproduced
24h/0h CPM ratio increase at all 4 loci (MYC SE 1.73x, MYC-490 1.05x, MYC-425 1.08x, MYC gene 1.10x)
within tolerance
V_track_concordance
Reported
(validation) reproduced vs authors' deposited BigWigs at MYC locus
Reproduced
fwd-vs-pos r=0.89-0.92; rev-vs-neg |r|=0.97-0.99; cross-strand ~0.10-0.13
within tolerance

Assessments & scoring basis

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Reproduction footprint

claude-opus-4-8

Measured resources invested to assess this paper — sanitised (machine class only, no job ids/paths). Compute = HPC accounting (SLURM); tokens = the AI agent's session.

963.1 k
tokens (I/O) · 72.2 M incl. cache
683 min
runtime
Per-job HPC accounting not captured for this run — the runtime shown is the reproduction’s measured wall-clock time.