Sissy Bassani’s poster on the “Variant‑specific pathophysiologicalmechanisms of AFF3”

Sissy Bassani (former member of group Reymond) received the of Best Poster runners-up Award at the 57th Annual Meeting of the European Society of Human Genetics, Berlin, Germany.

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Postdoctoral Fellowship & Mobility Funding Opportunities – Information Session – June 11, 2024

The EPFL Research Office, in collaboration with the UNIL Research Service, is pleased to invite you to an information session on Postdoc & Mobility Funding Opportunities.

You are affiliated to EPFL or UNIL, and you would like to know more about the funding opportunities available to you?

Then don’t miss our information session, which will be held on Tuesday, June 11, 2023, from 12:15 to 13:45

During this information session, you will have the opportunity to:

  • Discover the different funding opportunities in Switzerland, Europe and elsewhere, including program missions and eligibility criteria.
  • Familiarize yourself with the relevant institutional rules for the different scholarship programs.
  • Obtain valuable advice on the application process.
  • Participate in a question and answer session with experts from EPFL and UNIL.

Please note that registration is required, and that the session will be held in English.

Once your registration is confirmed, you will receive additional information about the event.

If you have additional questions or need more information, please do not hesitate to contact the EPFL Research Office at research@epfl.ch

The EPFL Research Office and the UNIL Research Service are looking forward to welcoming you at this information session.

Do not miss this opportunity to discover funding opportunities that could help you advance in your research career !

Biochim Biophys Acta Mol Cell Res, auth.: group Fajas

E2F transcription factor-1 modulates expression of glutamine metabolic genes in mouse embryonic fibroblasts and uterine sarcoma cells

Katharina Huber 1Albert Giralt 2René Dreos 2Helene Michenthaler 3Sarah Geller 2Valentin Barquissau 2Dorian V Ziegler 2Daniele Tavernari 4Hector Gallart-Ayala 5Katarina Krajina 6Katharina Jonas 6Giovanni Ciriello 4Julijana Ivanisevic 5Andreas Prokesch 7Martin Pichler 8Lluis Fajas 9

Affiliations expand

Free article

Abstract

Metabolic reprogramming is considered as a hallmark of cancer and is clinically exploited as a novel target for therapy. The E2F transcription factor-1 (E2F1) regulates various cellular processes, including proliferative and metabolic pathways, and acts, depending on the cellular and molecular context, as an oncogene or tumor suppressor. The latter is evident by the observation that E2f1-knockout mice develop spontaneous tumors, including uterine sarcomas. This dual role warrants a detailed investigation of how E2F1 loss impacts metabolic pathways related to cancer progression. Our data indicate that E2F1 binds to the promoter of several glutamine metabolism-related genes. Interestingly, the expression of genes in the glutamine metabolic pathway were increased in mouse embryonic fibroblasts (MEFs) lacking E2F1. In addition, we confirm that E2f1-/- MEFs are more efficient in metabolizing glutamine and producing glutamine-derived precursors for proliferation. Mechanistically, we observe a co-occupancy of E2F1 and MYC on glutamine metabolic promoters, increased MYC binding after E2F1 depletion and that silencing of MYC decreased the expression of glutamine-related genes in E2f1-/- MEFs. Analyses of transcriptomic profiles in 29 different human cancers identified uterine sarcoma that showed a negative correlation between E2F1 and glutamine metabolic genes. CRISPR/Cas9 knockout of E2F1 in the uterine sarcoma cell line SK-UT-1 confirmed elevated glutamine metabolic gene expression, increased proliferation and increased MYC binding to glutamine-related promoters upon E2F1 loss. Together, our data suggest a crucial role of E2F1 in energy metabolism and metabolic adaptation in uterine sarcoma cells.