Eventdetails

How cancer cells cope with tryptophan restriction

Type

• Vortrag

Topic

• Human & Biotechnology (Field of Expertise)
• Andere Forschungsthemen
• Kultur

On 18 January at 5 p.m. Prof. Kathrin Thedieck and Dr. Alexander Heberle will hold a Flagship Lecture at Graz University of Technology, Steyrergasse 30, Ground floor, Lecture Hall BE01.

Kathrin Thedieck (Professor at the Institute of Biochemistry, University of Innsbruck) und Alexander Martin Heberle (Junior Group Leader, Post-Doctoral Researcher at the Institut of Biochemistry at the University of Innsbruck) will speak on the following topics:

Kathrin Thedieck: “How cancer cells cope with tryptophan restriction”
Tryptophan (Trp) metabolism is increasingly being recognized to enhance tumor malignancy. Glioblastoma is a devastating tumor entity with few treatment options and they often exhibits enhanced levels of the Trp-degrading enzyme TDO2 (Trp 2,3-dioxygenase), resulting not only in increased amounts of oncogenic Trp metabolites that drive malignancy, but also in the depletion of the essential amino acid Trp. This seems to be at odds with the requirement of amino acids for protein biosynthesis in rapidly growing tumor cells; raising the question how cancer cells sustain growth when depleted of Trp. We unraveled a surprising mechanism that enables tumor cells to survive and grow when Trp is scarce. Our findings unveil unexpected vulnerabilities and open new avenues for therapy.

Alexander Martin Heberle: “A stress granule protein integrates metabolic signals and controls lysosomal TSC recruitment and mTORC1 suppression in breast cancer”
The tuberous sclerosis protein (TSC) complex acts as a relay for anabolic signaling and as a tumor suppressor. These functions are mediated via the inhibition of the metabolic master regulator mTORC1 (mechanistic target of rapamycin complex 1) at its central signaling platform – the lysosomes. We recently discovered that the stress granule protein G3BP1 (Ras GTPase-activating protein-binding protein 1) anchors the TSC complex to lysosomes needed for the suppression of mTORC1 by nutritional signals (PMID: 33497611). Using biochemical approaches and in silico predictions we find that the G3BP1-TSC axis mediates metabolic signals to mTORC1, suggesting a novel mode of TSC-mediated nutrient sensing.

You can register here for the event until 16 January: biotechmedgraz.at/facultyclub

Host

BioTechMed-Graz