@article{10712,
  abstract     = {Solute carriers are increasingly recognized as participating in a plethora of pathologies, including cancer. We describe here the involvement of the orphan solute carrier MFSD1 in the regulation of tumor cell migration. Loss of MFSD1 enabled higher levels of metastasis in a mouse model. We identified an increased migratory potential in MFSD1-/- tumor cells which was mediated by increased focal adhesion turn-over, reduced stability of mature inactive β1 integrin, and the resulting increased integrin activation index. We show that MFSD1 promoted recycling to the cell surface of endocytosed inactive β1 integrin and thereby protected β1 integrin from proteolytic degradation; this led to dampening of the integrin activation index. Furthermore, down-regulation of MFSD1 expression was observed during early steps of tumorigenesis and higher MFSD1 expression levels correlate with a better cancer patient prognosis. In sum, we describe a requirement for endolysosomal MFSD1 in efficient β1 integrin recycling to suppress tumor spread.},
  author       = {Roblek, Marko and Bicher, Julia and van Gogh, Merel and György, Attila and Seeböck, Rita and Szulc, Bozena and Damme, Markus and Olczak, Mariusz and Borsig, Lubor and Siekhaus, Daria E},
  issn         = {2234-943X},
  journal      = {Frontiers in Oncology},
  publisher    = {Frontiers},
  title        = {{The solute carrier MFSD1 decreases β1 integrin’s activation status and thus tumor metastasis}},
  doi          = {10.3389/fonc.2022.777634},
  volume       = {12},
  year         = {2022},
}

@article{12268,
  abstract     = {The complexity of the microenvironment effects on cell response, show accumulating evidence that glioblastoma (GBM) migration and invasiveness are influenced by the mechanical rigidity of their surroundings. The epithelial–mesenchymal transition (EMT) is a well-recognized driving force of the invasive behavior of cancer. However, the primary mechanisms of EMT initiation and progression remain unclear. We have previously showed that certain substrate stiffness can selectively stimulate human GBM U251-MG and GL15 glioblastoma cell lines motility. The present study unifies several known EMT mediators to uncover the reason of the regulation and response to these stiffnesses. Our results revealed that changing the rigidity of the mechanical environment tuned the response of both cell lines through change in morphological features, epithelial-mesenchymal markers (E-, N-Cadherin), EGFR and ROS expressions in an interrelated manner. Specifically, a stiffer microenvironment induced a mesenchymal cell shape, a more fragmented morphology, higher intracellular cytosolic ROS expression and lower mitochondrial ROS. Finally, we observed that cells more motile showed a more depolarized mitochondrial membrane potential. Unravelling the process that regulates GBM cells’ infiltrative behavior could provide new opportunities for identification of new targets and less invasive approaches for treatment.},
  author       = {Basilico, Bernadette and Palamà, Ilaria Elena and D’Amone, Stefania and Lauro, Clotilde and Rosito, Maria and Grieco, Maddalena and Ratano, Patrizia and Cordella, Federica and Sanchini, Caterina and Di Angelantonio, Silvia and Ragozzino, Davide and Cascione, Mariafrancesca and Gigli, Giuseppe and Cortese, Barbara},
  issn         = {2234-943X},
  journal      = {Frontiers in Oncology},
  keywords     = {Cancer Research, Oncology},
  publisher    = {Frontiers Media},
  title        = {{Substrate stiffness effect on molecular crosstalk of epithelial-mesenchymal transition mediators of human glioblastoma cells}},
  doi          = {10.3389/fonc.2022.983507},
  volume       = {12},
  year         = {2022},
}