GEO series

The methyltransferases METTL7A and METTL7B confer resistance of cancer cells to thiol-based histone deacetylate inhibitors (RNA-Seq)

GSE217127 Homo sapiens (human) RNA-seq (gene expression) 12 samples Submitted 2025/05/13 Platform GPL18573

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 × HuT78 DpVp RNAseq vs 3 × HuT78 Parental RNAseq vs 3 × MCF7 DpVp RNAseq vs 3 × MCF7 Parental RNAseqGroups 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: The Methyltransferases METTL7A and METTL7B Confer Resistance to Thiol-Based Histone Deacetylase InhibitorsMolecular cancer therapeutics · 2024

Summary (written by the submitters)

Histone deacetylase inhibitors (HDI) are among the growing class of epigenetic therapies used for the treatment of cancer. Although histone deacetylase inhibitors (HDIs) are effective in the treatment of T-cell lymphomas, solid tumors are largely resistant, and few mechanisms of resistance have been described. Overexpression of the multi-drug resistance gene ABCB1 that encodes P-glycoprotein (P-gp) is known to confer resistance to the HDI romidepsin, yet it is not associated with resistance in patients, suggesting other mechanisms of resistance arise in patients.

Read the full summary ↓

To identify alternative romidepsin resistance mechanisms, we selected MCF-7 breast cancer cells with romidepsin in the presence of verapamil to reduce the chance of P-gp over-expression developing as a resistance mechanism. The resulting subline, MCF-7 DpVp300, does not express P-gp and was found to be selectively resistant to romidpesin but not other HDIs such as belinostat, panobinostat, or vorinostat. RNA sequencing analysis demonstrated upregulation of the putative methyltransferase, METTL7A, a paralog of which, METTL7B, was found to methylate thiol groups on hydrogen sulfide and captopril. We hypothesized that METTL7A could methylate and inactivate romidepsin as well as other HDIs with a thiol as the zinc binding group. Here we show that expression of METTL7A is necessary for thiol-based HDI resistance in the MCF-7 DpVp300 cell line, and that expression of METTL7A or METTL7B in sensitive cells confers resistance to thiol based HDIs. We thus propose that METTL7A and METTL7B confer resistance to thiol-based HDIs by methylating and inactivating the zinc-binding thiol.

Published in

The Methyltransferases METTL7A and METTL7B Confer Resistance to Thiol-Based Histone Deacetylase Inhibitors

Robey RW, Fitzsimmons CM, Guiblet WM et al. · Molecular cancer therapeutics 2024 · PMID 38151817 · doi:10.1158/1535-7163.MCT-23-0144

This dataset

Open GSE217127 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 GSE217127_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 PRJNA896981 and SRA study SRP405938. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 38151817) ↗

Study design

3 × HuT78 DpVp RNAseq vs 3 × HuT78 Parental RNAseq vs 3 × MCF7 DpVp RNAseq vs 3 × MCF7 Parental RNAseq

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

GSM6705480 HuT78 DpVp RNAseq Replicate 1 HuT78 DpVp RNAseq
GSM6705481 HuT78 DpVp RNAseq Replicate 2 HuT78 DpVp RNAseq
GSM6705482 HuT78 DpVp RNAseq Replicate 3 HuT78 DpVp RNAseq
GSM6705483 HuT78 Parental RNAseq Replicate 1 HuT78 Parental RNAseq
GSM6705484 HuT78 Parental RNAseq Replicate 2 HuT78 Parental RNAseq
GSM6705485 HuT78 Parental RNAseq Replicate 3 HuT78 Parental RNAseq
GSM6705486 MCF7 DpVp RNAseq Replicate 1 MCF7 DpVp RNAseq
GSM6705487 MCF7 DpVp RNAseq Replicate 2 MCF7 DpVp RNAseq
GSM6705488 MCF7 DpVp RNAseq Replicate 3 MCF7 DpVp RNAseq
GSM6705489 MCF7 Parental RNAseq Replicate 1 MCF7 Parental RNAseq
GSM6705490 MCF7 Parental RNAseq Replicate 2 MCF7 Parental RNAseq
GSM6705491 MCF7 Parental RNAseq Replicate 3 MCF7 Parental RNAseq

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GSE217130 The methyltransferases METTL7A and METTL7B confer resistance of cancer cells to thiol-based histone deacetylate inhibitors 22 samples shares mettl7a, mettl7b, methyltransferases, thiol-based, deacetylate, resistance, inhibitors, histone
GSE217128 The methyltransferases METTL7A and METTL7B confer resistance of cancer cells to thiol-based histone deacetylate inhibitors (ATAC-Seq) 8 samples shares mettl7a, mettl7b, methyltransferases, thiol-based, deacetylate, resistance, inhibitors, histone
GSE217129 The methyltransferases METTL7A and METTL7B confer resistance of cancer cells to thiol-based histone deacetylate inhibitors (Mnase-Seq) 2 samples shares mettl7a, mettl7b, methyltransferases, thiol-based, deacetylate, resistance, inhibitors, histone
GSE281811 Combined inhibition of histone methyltransferases EZH2 and DOT1L is an effective therapy for neuroblastoma 16 samples shares methyltransferases, histone
GSE242328 METTL7B is an essential epigenetic regulator of lineage specification in glioblastoma [RNAseq] 16 samples shares mettl7b
GSE242966 METTL7B is an essential epigenetic regulator of lineage specification in glioblastoma [scRNAseq] 9 samples shares mettl7b
GSE243132 METTL7B is an essential epigenetic regulator of lineage specification in glioblastoma 73 samples shares mettl7b
GSE242326 METTL7B is an essential epigenetic regulator of lineage specification in glioblastoma [ChIPseq] 32 samples shares mettl7b

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