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

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

PROVIDER: PRJNA896983 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22148690_1.fastq.gz	Fastqsanger.gz
	SRR22148690_2.fastq.gz	Fastqsanger.gz
	SRR22148691_1.fastq.gz	Fastqsanger.gz
	SRR22148691_2.fastq.gz	Fastqsanger.gz

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Similar Datasets

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

Project description: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. 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.

2025-05-13 | GSE217129 | GEO

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

2025-05-13 | GSE217128 | GEO

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

2025-05-13 | GSE217127 | GEO

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

Project description:The methyltransferases METTL7A and METTL7B confer resistance of cancer cells to thiol-based histone deacetylate inhibitors

| PRJNA896986 | ENA

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

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

| PRJNA896984 | ENA

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

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

| PRJNA896981 | ENA

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

Project description:Histone deacetylase inhibitors (HDACi) are part of a growing class of epigenetic therapies used for the treatment of cancer. Although HDACis are effective in the treatment of T-cell lymphomas, treatment of solid tumors with this class of drugs has not been successful. Overexpression of the multidrug resistance protein P-glycoprotein (P-gp), encoded by ABCB1, is known to confer resistance to the HDACi romidepsin in vitro, yet increased ABCB1 expression has not been associated with resistance in patients, suggesting that other mechanisms of resistance arise in the clinic. To identify alternative mechanisms of resistance to romidepsin, we selected MCF-7 breast cancer cells with romidepsin in the presence of the P-gp inhibitor verapamil to reduce the likelihood of P-gp-mediated resistance. The resulting cell line, MCF-7 DpVp300, does not express P-gp and was found to be selectively resistant to romidepsin but not to other HDACis such as belinostat, panobinostat, or vorinostat. RNA-sequencing analysis revealed upregulation of the mRNA coding for the putative methyltransferase, METTL7A, whose paralog, METTL7B, was previously shown to methylate thiol groups on hydrogen sulfide and captopril. As romidepsin has a thiol as the zinc-binding moiety, we hypothesized that METTL7A could inactivate romidepsin and other thiol-based HDACis via methylation of the thiol group. We demonstrate that expression of METTL7A or METTL7B confers resistance to thiol-based HDACis and that both enzymes are capable of methylating thiol-containing HDACis. We thus propose that METTL7A and METTL7B confer resistance to thiol-based HDACis by methylating and inactivating the zinc-binding thiol.

| S-EPMC11223745 | biostudies-literature

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

Project description:This SuperSeries is composed of the SubSeries listed below.

2025-05-14 | GSE217130 | GEO

METTL7A improves bovine embryo competence by attenuating oxidative stress

Project description:In vitro fertilization (IVF) is currently one of the most used assisted reproductive technologies to achieve a successful pregnancy. However, the acquisition of oxidative stress in embryo in vitro culture impairs its competence. Here, we demonstrated that the S-adenosyl-L-methionine (SAMe)-dependent thiol methyltransferase, methyltransferase-like protein 7A (METTL7A) improves the developmental potential of bovine embryos. We found exogenous METTL7A modulates expression of genes involved in embryonic cell mitochondrial pathways and promotes trophectoderm development. Surprisingly, we discovered that METTL7A alleviates mitochondrial stress and DNA damage and promotes cell cycle progression during embryo cleavage. In summary, we have identified a novel mitochondria stress eliminate mechanism regulated by METTL7A that occurs during the acquisition of oxidative stress in embryo in vitro culture. This discovery lays the groundwork for the development of METTL7A as a promising therapeutic target for IVF embryo competence.

2025-02-12 | GSE272473 | GEO

METTL7B is an essential epigenetic regulator of lineage specification in glioblastoma [RNAseq]

Project description:Glioblastomas are the most common malignant brain tumours in adults; they are highly aggressive, heterogeneous and plastic. We have identified METTL7B as an essential regulator of lineage specification in glioblastoma, with impact on both tumour size and invasiveness in in vivo models. Single cell transcriptomic analysis of these tumours and of cerebral organoids derived from expanded potential stem cells overexpressing METTL7B identified a regulatory role for the gene in the neural stem cells to astrocyte differentiation trajectory. Mechanistically, METTL7B downregulates the expression of key neuronal differentiation players, including SALL2, via DNA methylation and post-translational modifications of histone marks.

2024-07-01 | GSE242328 | GEO

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