@article{mariant_bacola_van landeghem_2023, title={Mini-Review: Enteric glia of the tumor microenvironment: An affair of corruption}, volume={814}, ISSN={["1872-7972"]}, DOI={10.1016/j.neulet.2023.137416}, abstractNote={The tumor microenvironment corresponds to a complex mixture of bioactive products released by local and recruited cells whose normal functions have been “corrupted” by cues originating from the tumor, mostly to favor cancer growth, dissemination and resistance to therapies. While the immune and the mesenchymal cellular components of the tumor microenvironment in colon cancer have been under intense scrutiny over the last two decades, the influence of the resident neural cells of the gut on colon carcinogenesis has only very recently begun to draw attention. The vast majority of the resident neural cells of the gastrointestinal tract belong to the enteric nervous system and correspond to enteric neurons and enteric glial cells, both of which have been understudied in the context of colon cancer development and progression. In this review, we especially discuss available evidence on enteric glia impact on colon carcinogenesis. To highlight “corrupted” functioning in enteric glial cells of the tumor microenvironment and its repercussion on tumorigenesis, we first review the main regulatory effects of enteric glial cells on the intestinal epithelium in homeostatic conditions and we next present current knowledge on enteric glia influence on colon tumorigenesis. We particularly examine how enteric glial cell heterogeneity and plasticity require further appreciation to better understand the distinct regulatory interactions enteric glial cell subtypes engage with the various cell types of the tumor, and to identify novel biological targets to block enteric glia pro-carcinogenic signaling.}, journal={NEUROSCIENCE LETTERS}, author={Mariant, Chloe L. and Bacola, Gregory and Van Landeghem, Laurianne}, year={2023}, month={Sep} }
 @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. Tumor cells hijack enteric glia to activate colon cancer stem cells and stimulate tumorigenesisAltogether, 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. Full-Text PDF Open Access}, 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={BackgroundColon 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.MethodsImpact 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.FindingsOur 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.InterpretationAltogether, 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.FundingThis 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} }