Marcia C. Haigis

  • Latest publications

    Finley LW, Carracedo A, Lee J, Souza A, Egia A, Zhang J, Teruya-Feldstein J, Moreira PI, Cardosa SM, Clish CB, Pandolfi PP, Haigis MC. SIRT3 opposes reprogramming of cancer cell metabolism through HIF1alpha destabilization. Cancer Cell. 2011; 19:416-428. PMCID: PMC3065720.

    Jeong SM, Xiao C, Finley LW, Lahusen T, Souza AL, Pierce K, Li YH, Wang X, Laurent G, German, NJ, Xu X, Li C, Wang RH, Lee J, Csibi A, Cerione R, Blenis J, Clish CB, Kimmelman A, Deng CX, Haigis MC. SIRT4 has tumor-suppressive activity and regulates the cellular metabolic response to DNA damage by inhibiting mitochondrial glutamine metabolism. 2013. Cancer Cell, 23:450-463. PMCID: PMC3650305.

    Laurent G, German NJ, Saha AK, deBoer VCJ, Davies M, Koves TR, Dephoure N, Fischer F, Boanca G, Vaitheesvaran B, Lovitch SB, Sharpe AH, Kurland IJ, Steegborn C, Gygi SP, Muoio DM, Ruderman NB, Haigis MC. SIRT4 orchestrates the balance between lipid synthesis and catabolism by repressing malonyl-CoA decarboxylase. 2013. Molecular Cell, 5:686-698. Cover Article. PMCID: PMC3721068.

    Jeong SM, Lee J, Finley LW, Schmidt PJ, Fleming MD, Haigis MC. SIRT3 regulates cellular iron metabolism and cancer growth by repressing iron regulatory protein 1. Oncogene. 2014 Jun 9. PMID: 24909164

    German NJ, Haigis MC. Sirtuins and the Metabolic Hurdles in Cancer. Curr Biol. 2015. 25:R569-583. Review. PMID: 26126285.

  • Prizes and Awards

    American Cancer Society New Scholar Award, 2011

    Friedreich’s Ataxia Research Alliance Award, 2010

    Stewart Trust Award, 2010

    Catalyst Award, 2010

    Ellison Medical Foundation New Scholar Award, 2009

    Muscular Dystrophy Association Award, 2008

    Armenise-Harvard Junior Faculty Grant, Department of Pathology: “Characterization of SIRT5 function in protein repair and its links to metabolism and aging.” , 2007

     Brookdale Leadership in Aging Fellowship, 2007

    Carolyn and Peter S. Lynch Award, 2007

Who she is

Marcia C. Haigis obtained her Ph.D. in Biochemistry from the University of Wisconsin in 2002. She then performed postdoctoral research at MIT studying the biology of aging and mitochondrial metabolism. In 2006, Dr. Haigis joined the faculty of Harvard Medical School, where she is currently an Associate Professor in the Department of Cell Biology. Additionally, Dr. Haigis is an active member of the Paul F. Glenn Laboratories for Medical Research.

What she does

An overarching goal of the Haigis lab is to understand the role that mitochondria play in human health, aging and age-related diseases. In particular, the lab is working to identify new molecular mechanisms that allow mitochondria to mediate cellular adaptation to stress.

These studies have led to a deeper understanding of how mitochondria reprogram metabolism in response to cellular stress and identification of novel molecular mechanisms involved in this reprogramming. In their work, Haigis lab researchers have discovered new physiological processes regulated by mitochondrial sirtuins, which function as NAD-dependent deacetylases, deacylases or ADP-ribosyltransferases.

For example, using a platform of metabolomics, signaling, mitochondrial biochemistry and cell biology, the group has discovered that the mitochondrial deacetylase SIRT3 represses the Warburg effect in tumor cells, controlling cancer cell metabolism via a mitochondrial signaling pathway. These studies have the potential to lead to novel therapies that could treat a spectrum of human diseases.

News from the Lab

Recent studies in the Haigis laboratory have focused on elucidating metabolic reprogramming that allows cells to adapt to stress. The team has discovered a novel, ‘metabolic checkpoint’ that is induced in cells upon exposure to DNA damage. Many tumor cells undergo metabolic reprograming of glutamine metabolism, which provides precursors to support increased biosynthesis and redox control. Haigis lab’s work showed that cells lacking this metabolic checkpoint in response to stress experience high levels of genomic instability and transformation. The lab’s researchers are continuing this work to identify new molecular regulators that link mitochondria with metabolic checkpoints.