@article{vales_bacola_biraud_bessard_geraldo_dougherty_lashani_bossard_flamant_duchalais_et al._2023, title={Tumor cells hijack enteric glia to activate colon cancer stem cells and stimulate tumorigenesis (vol 49, pg 172, 2019)}, volume={88}, ISSN={["2352-3964"]}, DOI={10.1016/j.ebiom.2023.104448}, abstractNote={The publisher regrets that due to a production error, supplemental figures were accidentally omitted from the published version of this research paper. The original article has been updated. The publisher would like to apologise for any inconvenience caused.}, journal={EBIOMEDICINE}, author={Vales, Simon and Bacola, Gregory and Biraud, Mandy and Bessard, Anne and Geraldo, Fanny and Dougherty, Kelsie A. and Lashani, Shaian and Bossard, Celine and Flamant, Mathurin and Duchalais, Emilie and et al.}, year={2023}, month={Feb} }
 @article{aureille_buffiere-ribot_harvey_boyault_pernet_andersen_bacola_balland_fraboulet_van landeghem_et al._2019, title={Nuclear envelope deformation controls cell cycle progression in response to mechanical force}, volume={20}, ISSN={["1469-3178"]}, DOI={10.15252/embr.201948084}, abstractNote={The shape of the cell nucleus can vary considerably during developmental and pathological processes; however, the impact of nuclear morphology on cell behavior is not known. Here, we observed that the nuclear envelope flattens as cells transit from G1 to S phase and inhibition of myosin II prevents nuclear flattening and impedes progression to S phase. Strikingly, we show that applying compressive force on the nucleus in the absence of myosin II-mediated tension is sufficient to restore G1 to S transition. Using a combination of tools to manipulate nuclear morphology, we observed that nuclear flattening activates a subset of transcription factors, including TEAD and AP1, leading to transcriptional induction of target genes that promote G1 to S transition. In addition, we found that nuclear flattening mediates TEAD and AP1 activation in response to ROCK-generated contractility or cell spreading. Our results reveal that the nuclear envelope can operate as a mechanical sensor whose deformation controls cell growth in response to tension.}, number={9}, journal={EMBO REPORTS}, author={Aureille, Julien and Buffiere-Ribot, Valentin and Harvey, Ben E. and Boyault, Cyril and Pernet, Lydia and Andersen, Tomas and Bacola, Gregory and Balland, Martial and Fraboulet, Sandrine and Van Landeghem, Laurianne and et al.}, year={2019}, month={Sep} }
 @article{tumor cells hijack enteric glia to activate colon cancer stem cells and stimulate tumorigenesis._2019, url={https://doi.org/10.1016/j.ebiom.2019.09.045}, DOI={10.1016/j.ebiom.2019.09.045}, abstractNote={Colon cancer stem cells (CSCs), considered responsible for tumor initiation and cancer relapse, are constantly exposed to regulatory cues emanating from neighboring cells present in the tumor microenvironment. Among these cells are enteric glial cells (EGCs) that are potent regulators of the epithelium functions in a healthy intestine. However, whether EGCs impact CSC-driven tumorigenesis remains unknown.Impact of human EGC primary cultures or a non-transformed EGC line on CSCs isolated from human primary colon adenocarcinomas or colon cancer cell lines with different p53, MMR system and stemness status was determined using murine xenograft models and 3D co-culture systems. Supernatants of patient-matched human primary colon adenocarcinomas and non-adjacent healthy mucosa were used to mimic tumor versus healthy mucosa secretomes and compare their effects on EGCs.Our data show that EGCs stimulate CSC expansion and ability to give rise to tumors via paracrine signaling. Importantly, only EGCs that were pre-activated by tumor epithelial cell-derived soluble factors increased CSC tumorigenicity. Pharmacological inhibition of PGE2 biosynthesis in EGCs or IL-1 knockdown in tumor epithelial cells prevented EGC acquisition of a pro-tumorigenic phenotype. Inhibition of PGE2 receptor EP4 and EGFR in CSCs inhibited the effects of tumor-activated EGCs.Altogether, our results show that EGCs, once activated by the tumor, acquire a pro-tumorigenic phenotype and stimulate CSC-driven tumorigenesis via a PGE2/EP4/EGFR-dependent pathway.This work was supported by grants from the French National Cancer Institute, La Ligue contre le Cancer, the 'Région des Pays de la Loire' and the UNC Lineberger Comprehensive Cancer Center.}, journal={EBioMedicine}, year={2019}, month={Oct} }