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Inhibition of SIRT7 Overcomes Radioresistance in Pancreatic Neuroendocrine Tumors by Reactivating MEN1 Expression

GSE323363 Homo sapiens (human) RNA-seq (gene expression) 12 samples Submitted 2026/07/15 Platform GPL24676
At a glance

RNA-seq (gene expression) · human · 12 samples

What it is
RNA-seq (gene expression)Gene activity measured by sequencing. The summary does not mention single-cell work, so this is most likely bulk: one average per sample, the usual starting point for comparing groups.
Organism
Homo sapiens (human)
Samples
12 samples: 3 × QGP-1 cells, shControl vs 3 × QGP-1 cells, shSIRT7 vs 3 × BON-1 cells, Parental vs 3 × BON-1 cells, RadioresistantGroups are read from the sample names, not from the paper. Check the list below.
Data you can get
A processed table (series matrix) and supplementary files from NCBI; the raw sequencing reads from ENA. Which of these hold counts depends on the study, so check the file list.
Paper
Inhibition of SIRT7 Overcomes Radioresistance in Pancreatic Neuroendocrine Tumors by Reactivating MEN1 ExpressionAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
Summary (written by the submitters)
Pancreatic neuroendocrine tumors (PanNETs) frequently exhibit loss or reduced expression of the tumor suppressor MEN1, a key regulator of tumor progression and DNA damage response (DDR). However, the upstream mechanisms driving MEN1 silencing remain unclear. Here, a pooled epigenetic CRISPR–Cas9 screen identified the NAD⁺-dependent deacetylase SIRT7 as a critical suppressor of MEN1 expression.
Read the full summary ↓
Mechanistically, SIRT7 interacts with DNMT1 and promotes catalytic activity–dependent recruitment of DNMT1 to the MEN1 promoter, leading to promoter hypermethylation and transcriptional repression. Clinically, SIRT7 is overexpressed in PanNET tissues and inversely correlates with MEN1 levels and patient prognosis. Genetic or pharmacologic inhibition of SIRT7 restored MEN1 expression, reduced MRN complex abundance, and impaired double-strand break repair. Graded MEN1 re-expression demonstrated a quantitative relationship between MEN1 levels, DNA repair efficiency, and radiosensitivity. Functionally, SIRT7 inhibition enhanced radiation-induced DNA damage and apoptosis in a partially MEN1-dependent manner and significantly suppressed tumor growth in patient-derived organoids and multiple independent xenograft models. Collectively, these findings define a catalytic activity–dependent SIRT7–DNMT1–MEN1 epigenetic axis that modulates DDR and radiosensitivity, supporting SIRT7 targeting as a strategy to improve radiotherapy efficacy in PanNETs.
Published in
Inhibition of SIRT7 Overcomes Radioresistance in Pancreatic Neuroendocrine Tumors by Reactivating MEN1 Expression
Jiang J, Wang Y, Qin Y et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) 2026 · PMID 41972414 · doi:10.1002/advs.202519824
This dataset
Open GSE323363 in finder → Find more human RNA-seq datasets →
Download · which file do I need?

Direct links to NCBI and ENA, no account and no request form. Pick by what you want to do: take the small processed table to look, the supplementary files to re-analyse, or the original raw data to start over.

1 · Just have a look

Processed table

The series matrix: one table of values per sample as the submitters processed it. The smallest download, and it opens in Excel or R. Start here to see what the data look like.

Series matrix ↓
2 · Re-analyse it

Supplementary files

The count tables and other files the authors uploaded. Take only the samples you need, or the whole study as GSE323363_RAW.tar (it can run to tens of gigabytes).

All supplementary files ↗ Whole study · RAW.tar ↓
3 · Start from the raw reads

Raw sequencing reads

The original FASTQ files, straight from the sequencer, held at ENA. Large, and you align them yourself, so only choose this if you need to re-process the study from scratch.

Raw reads on ENA ↗

What the files usually look like: For RNA-seq the counts are usually a table among the supplementary files (look for 'counts', 'expression', 'FPKM' or 'TPM' in the file name). The series matrix of a sequencing study is sometimes nearly empty.

Also filed as BioProject PRJNA1432533 and SRA study SRP681170. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 41972414) ↗
Study design
3 × QGP-1 cells, shControl vs 3 × QGP-1 cells, shSIRT7 vs 3 × BON-1 cells, Parental vs 3 × BON-1 cells, Radioresistant

Supports a between-group comparison across 12 samples.

How we read this: 4 replicated groups read from 12 sample titles; they account for 12 of them. These groups are guessed from the sample names, not taken from the paper, so check them against the sample list below before relying on them.

Samples in this study
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