Silvia Rodriguez Marin

Abstract Several mechanisms of resistance of cancer cells to cyclin-dependent kinase inhibitors (CDKi) have been identified, including the upregulation of metabolic regulators such as glutaminase. However, whether such resistance mechanisms represent optimal targets has not been determined. Here, we have systematically analyzed metabolic reprogramming in colorectal cancer cells exposed to Palbociclib, a CDKi selectively targeting CDK4/6, or Telaglenastat, a selective glutaminase inhibitor.

1 INTRODUCTION Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is responsible for over 770 million cases of coronavirus disease 2019 (COVID-19) and over 7 million deaths since its emergence in 2019/2020.1 Upon infecting susceptible cells, SARS-CoV-2 subverts and disables innate immune responses and, simultaneously, hijacks metabolic pathways to favor viral replication and production at the expense of the infected cell.