Yasaman Heidarian
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Yasaman Heidarian has a total of 22 co-authors. Here are the top co-authors by number of shared publications:
- Alexander J. Fitt
Department of Biology, Indiana University, Bloomington, Indiana, USA
1 shared publication - Anirban Kundu
Department of Urology, The University of Arizona Cancer Center, University of Arizona, Tucson, AZ 85721, United States of America
1 shared publication - David K. Crossman
Department of Genetics, University of Alabama at Birmingham, Birmingham, AL 35294, USA
1 shared publication - Devin M. Absher
HudsonAlpha Institute for Biotechnology, Huntsville, Alabama
1 shared publication - Dinesh Rakheja
Department of Pathology, University of Texas Southwestern Medical Center, Dallas, USA
1 shared publication - EunHee Shim
Department of Urology, University of Alabama at Birmingham, Birmingham, Alabama, USA
1 shared publication
Latest Publications
- Open Access
- 14 May 2024
- Published by American Society for Clinical Investigation in Journal of Clinical Investigation
- Vol. 134 (13)
l-2-Hydroxyglutarate remodeling of the epigenome and epitranscriptome creates a metabolic vulnerability in kidney cancer models
Tumor cells are known to undergo considerable metabolic reprogramming to meet their unique demands and drive tumor growth. At the same time, this reprogramming may come at a cost with resultant metabolic vulnerabilities. The small molecule l-2-hydroxyglutarate (l-2HG) is elevated in the most common histology of renal cancer. Similarly to other oncometabolites, l-2HG has the potential to profoundly impact gene expression. Here, we demonstrate that l-2HG remodels amino acid metabolism in renal cancer cells through combined effects on histone methylation and RNA N 6 -methyladenosine. The combined effects of l-2HG result in a metabolic liability that renders tumors cells reliant on exogenous serine to support proliferation, redox homeostasis, and tumor growth. In concert with these data, high–l-2HG kidney cancers demonstrate reduced expression of multiple serine biosynthetic enzymes. Collectively, our data indicate that high–l-2HG renal tumors could be specifically targeted by strategies that limit serine availability to tumors.
- 14 May 2024
- Published by American Society for Clinical Investigation in Journal of Clinical Investigation
- Vol. 134 (13)
Open Accessl-2-Hydroxyglutarate remodeling of the epigenome and epitranscriptome creates a metabolic vulnerability in kidney cancer models
Tumor cells are known to undergo considerable metabolic reprogramming to meet their unique demands and drive tumor growth. At the same time, this reprogramming may come at a cost with resultant metabolic vulnerabilities. The small molecule l-2-hydroxyglutarate (l-2HG) is elevated in the most common histology of renal cancer. Similarly to other oncometabolites, l-2HG has the potential to profoundly impact gene expression. Here, we demonstrate that l-2HG remodels amino acid metabolism in renal cancer cells through combined effects on histone methylation and RNA N 6 -methyladenosine. The combined effects of l-2HG result in a metabolic liability that renders tumors cells reliant on exogenous serine to support proliferation, redox homeostasis, and tumor growth. In concert with these data, high–l-2HG kidney cancers demonstrate reduced expression of multiple serine biosynthetic enzymes. Collectively, our data indicate that high–l-2HG renal tumors could be specifically targeted by strategies that limit serine availability to tumors.