###### Abstract  
The direct impact of microgravity exposure on male germ cells, as well as on their malignant counterparts, has not been largely studied. In previous works, we reported our findings on a cell line derived from a human seminoma lesion (TCam-2 cell line) showing that acute exposure to simulated microgravity altered microtubule orientation, induced autophagy, and modified cell metabolism stimulating ROS production. Moreover, we demonstrated that the antioxidant administration prevented both TCam-2 microgravity-induced microtubule disorientation and autophagy induction. Herein, expanding previous investigations, we report that simulated microgravity exposure for 24 h induced the appearance, at an ultrastructural level, of cell-to-cell junctional contacts that were not detectable in cells grown at 1 g. In line with this result, pan-cadherin immunofluorescence analyzed by confocal microscopy, revealed the clustering of this marker at the plasma membrane level on microgravity exposed TCam-2 cells. The upregulation of cadherin was confirmed by Western blot analyses. Furthermore, we demonstrated that the microgravity-induced ROS increase was responsible for the distribution of cadherin nearby the plasma membrane, together with beta-catenin since the administration of antioxidants prevented this microgravity-dependent phenomenon. These results shed new light on the microgravity-induced modifications of the cell adhesive behavior and highlight the role of ROS as microgravity activated signal molecules. T 28 October  
knowledge revealing the tight interplay among mechanical forces, cell metabolism, and cell behavior [27???? ], as well as to put a spotlight on the importance of physical forces on cell physiology. To this concern, microgravity-related cell modifications have been studied generating an increasing body of evidence, which indicates how different aspects of cell physiology are tightly connected with the gravitational force [7??????????]. Indeed, several studies indicated that mammalian cells are able to perceive gravitational force, even if not \"mechano-sensitive cells\", and respond to the changes of gravitational force [7??????]. Among them, male germ cells have been revealed to be sensitive to changes of gravitational force [7??????????]. Our group focused the attention on TCam-2 cells, derived from a seminoma lesion, that through their malignant transformation, maintain at least partially the phenotypic and molecular features of their normal counterpart [???? ]. For this reason, this represents the best in vitro model to study testicular mitotically active male germ cells. In previous papers, we reported that microgravity transiently modified structural features of TCam-2 cells, such as cell shape, microtubule organization, and mitochondria morphology, and that these changes came together with the modification of some crucial cell activities. Indeed, we reported that simulated microgravity impaired the TCam-2 cell proliferation rate, promoted autophagy, modified some metabolic parameters, and stimulated reactive oxygen species (ROS) production [????]. Notably, we also demonstrated that the microgravity-dependent ROS increase is essential to trigger microgravity-induced TCam-2 cell autophagy and microtubule disorientation, since the administration of antioxidants counteracted these microgravity-dependent cellular responses [?? ]. In light of these results, the observed ROS production by TCam-2 cells after simulated microgravity exposure is used as molecular signals that allow cells to react to microenvironmental stress. In the present paper, expanding the already mentioned studies, we evaluated the effect of short-term exposure to simulated microgravity on TCam-2 cell junctional features at the ultrastructural and molecular level. We evaluated beta1 integrin as a marker of the cell to substrate interaction, whereas cadherin and beta-catenin have been studied as markers of the cell-to-cell junctional capability, and possible modulators of cell malignant behavior [????].