NSD3-Short Promotes Migration of A549 Lung Cancer Cells
SGC Open Notebook Project to Characterize the HMTase NSD3
Exp025 Objective: In a previous experiment (exp024), we observed an increase in E-cadherin expression in response to knockdown of the short isoform of NSD3. To determine if this change is functionally relevant, we performed wound healing assays to measure any corresponding alteration in the migratory potential of A549 lung epithelial cancer cells.
Funding Acknowledgment: The SGC is a registered charity (number 1097737) that receives funds from AbbVie, Bayer Pharma AG, Boehringer Ingelheim, Canada Foundation for Innovation, Eshelman Institute for Innovation, Genome Canada through Ontario Genomics Institute [OGI-055], Innovative Medicines Initiative (EU/EFPIA) [ULTRA-DD grant no. 115766], Janssen, Merck KGaA, Darmstadt, Germany, MSD, Novartis Pharma AG, Ontario Ministry of Research, Innovation and Science (MRIS), Pfizer, São Paulo Research Foundation-FAPESP, Takeda, and Wellcome.