José M. González Dalmasy
A5069124762- Epigenetics and DNA Methylation
- Histone Deacetylase Inhibitors Research
- Cancer-related gene regulation
- Drug Transport and Resistance Mechanisms
- Ferroptosis and cancer prognosis
- Adenosine and Purinergic Signaling
- MicroRNA in disease regulation
National Cancer Institute
2022-2024
Center for Cancer Research
2022-2024
National Institutes of Health
2022-2024
Aim: Ferroptosis is a non-apoptotic form of cell death caused by lethal lipid peroxidation. Several small molecule ferroptosis inducers (FINs) have been reported, yet little information available regarding their interaction with the ATP-binding cassette (ABC) transporters P-glycoprotein (P-gp, ABCB1) and ABCG2. We thus sought to characterize interactions FINs P-gp ABCG2, which may provide oral bioavailability brain penetration predict drug-drug interactions. Methods: Cytotoxicity assays...
Abstract Histone deacetylase inhibitors (HDACi) are part of a growing class epigenetic therapies used for the treatment cancer. Although HDACis effective in T-cell lymphomas, solid tumors with this drugs has not been successful. Overexpression multidrug resistance protein P-glycoprotein (P-gp), encoded by ABCB1, is known to confer HDACi romidepsin vitro, yet increased ABCB1 expression associated patients, suggesting that other mechanisms arise clinic. To identify alternative romidepsin, we...
ABSTRACT Histone deacetylase inhibitors (HDACis) are part of a growing class epigenetic therapies used for the treatment cancer. While elevated levels efflux pump P-gp associated with in vitro resistance to romidepsin, this mechanism does not translate clinic. We developed romidepsin-resistant cell line independent function that acts upstream deacetylation process. found expression methyltransferase METTL7A is necessary resistance, and naïve cells can drive thiol-containing HDACis....
Ferroptosis is a form of cell death caused by direct or indirect inhibition glutathione peroxidase 4 that leads to lethal lipid peroxidation. Several small molecule ferroptosis inducers (FINs) have been reported, yet little information available regarding resistance mechanisms, particularly their interaction with the ATP-binding cassette (ABC) transporters P-glycoprotein (P-gp, ABCB1) and ABCG2. Given role ABC play in absorption, distribution, excretion many drugs, characterizing these...
ABSTRACT Although few resistance mechanisms for histone deacetylase inhibitors (HDACis) have been described, we recently demonstrated that TMT1A (formerly METTL7A) and TMT1B METTL7B) can mediate to HDACis with a thiol as the zinc-binding group by methylating inactivating drug. are poorly characterized, their normal physiological role has yet be determined. As animal model systems often used determine function of proteins, investigated whether ability these methyltransferases methylate...
<p>Supplemental Table S8 contains information about METTL7A and METTL7B in T-cell lymphoma tissue microarray samples</p>
<p>Supplemental Table S2 contains information about the cross-resistance profile of MCF7 DpVp300 cells for multiple drugs</p>
<p>Figure S2 contains cell cycle analysis and cytotoxicity data for MCF7 DpVp300 cells showing they are resistant to romidepsin do not overexpress P-gp</p>
<p>Figure S1 contains chemical structures of select HDAC inhibitors</p>
<p>Supplemental Table S8 contains information about METTL7A and METTL7B in T-cell lymphoma tissue microarray samples</p>
<p>Supplemental Table S7 contains information about the normal tissue expression of METTL7A and METTL7B</p>
<p>Figure S3 contains gene ontology analysis, motif and nucleosome density from the RNA-seq ATAC-seq data.</p>
<p>Figure S4 contains cytotoxicity assay and immunoblot data from the MCF7 DpVp300 cell lines showing that expression of METTL7A confers resistance.</p>
<p>Figure S1 contains chemical structures of select HDAC inhibitors</p>
<p>Supplemental Table S1 contains information about the chemical structures of HDACi</p>
<p>Figure S2 contains cell cycle analysis and cytotoxicity data for MCF7 DpVp300 cells showing they are resistant to romidepsin do not overexpress P-gp</p>
<div>Abstract<p>Histone deacetylase inhibitors (HDACi) are part of a growing class epigenetic therapies used for the treatment cancer. Although HDACis effective in T-cell lymphomas, solid tumors with this drugs has not been successful. Overexpression multidrug resistance protein P-glycoprotein (P-gp), encoded by <i>ABCB1</i>, is known to confer HDACi romidepsin <i>in vitro</i>, yet increased <i>ABCB1</i> expression associated patients,...
<div>Abstract<p>Histone deacetylase inhibitors (HDACi) are part of a growing class epigenetic therapies used for the treatment cancer. Although HDACis effective in T-cell lymphomas, solid tumors with this drugs has not been successful. Overexpression multidrug resistance protein P-glycoprotein (P-gp), encoded by <i>ABCB1</i>, is known to confer HDACi romidepsin <i>in vitro</i>, yet increased <i>ABCB1</i> expression associated patients,...
<p>Figure S6 contains cell cycle analysis of cells overexpressing METTL7A.</p>
<p>Figure S4 contains cytotoxicity assay and immunoblot data from the MCF7 DpVp300 cell lines showing that expression of METTL7A confers resistance.</p>
<p>Figure S3 contains gene ontology analysis, motif and nucleosome density from the RNA-seq ATAC-seq data.</p>
<p>Supplemental Table S3 contains information from high-throughput sequencing</p>
<p>Figure S5 contains cycle analysis of MCF7 DpVp300 cells following knockdown METTL7A.</p>
<p>Supplemental Table S1 contains information about the chemical structures of HDACi</p>
<p>Figure S5 contains cycle analysis of MCF7 DpVp300 cells following knockdown METTL7A.</p>