SLC35F2 Knockout Cell Line (HCT 116)

The choice depends on whether you are studying SLC35F2's role as a cellular uptake transporter for the cytotoxic compound YM155 (sepantronium bromide) or its emerging endogenous functions. The Knockout line is the standard tool for asking whether SLC35F2 is required for cellular YM155 uptake — SLC35F2 was identified through CRISPR screens as the principal transporter responsible for YM155 sensitivity, and its loss confers strong YM155 resistance. Overexpression is useful for studying YM155-targeted drug delivery strategies. For drug development research, the EDITGENE SLC35F2 Knockout in HCT 116 is particularly valuable — YM155 is being investigated for solid tumors and lymphomas, and SLC35F2 expression directly predicts YM155 sensitivity. Rescue with wild-type SLC35F2 restores YM155 sensitivity in resistant cells — this rescue paradigm is the established positive control. Rescue with transport-deficient variants enables structure-function studies.

Primary applications: • YM155 sensitivity assays: cell viability dose-response analysis for YM155 (sepantronium bromide) in SLC35F2-null versus rescued cells — the gold standard for confirming SLC35F2-dependent drug uptake. • YM155 uptake assays: LC-MS quantification of intracellular YM155 accumulation. • Anti-cancer ADC and prodrug research: characterization of other SLC35F2-substrate compounds in development for solid tumors and lymphomas. • Biomarker validation: SLC35F2 expression analysis as a predictive biomarker for YM155 response in patient samples. EDITGENE recommends this model for researchers investigating YM155 pharmacology, drug uptake mechanisms, and SLC35F2-substrate compound development.

Yes. SLC35F2 rescue experiments are well-established for YM155 drug uptake research: • Construct design: use a codon-modified SLC35F2 sequence with a small C-terminal tag (FLAG, HA). The 10 transmembrane SLC35 architecture must be preserved. • YM155 sensitivity restoration: rescue with wild-type SLC35F2 in YM155-resistant cells (e.g., the knockout) restores drug sensitivity — the established positive control paradigm. • Transport-deficient rescue: substrate-binding pocket mutations enable distinguishing transport activity from non-transport functions. • Functional readout: rescue should restore YM155-induced cytotoxicity (IC50 measurements) and intracellular YM155 accumulation (LC-MS). HCT 116 transduces efficiently with lentivirus and supports stable rescue line generation.