SLC16A7 Knockout Cell Line (HCT 116)

The choice depends on whether you are studying SLC16A7 (MCT2)'s role as a high-affinity monocarboxylate transporter or its specific contributions distinct from MCT1 (SLC16A1) and MCT4 (SLC16A3). The Knockout line is the standard tool for asking whether MCT2 is required for lactate, pyruvate, and ketone body transport in contexts where MCT2 dominates over other MCT family members. Overexpression is useful for studying MCT2 in heterologous systems or for testing inhibitor selectivity. For monocarboxylate transport research, the EDITGENE MCT2 Knockout in HCT 116 enables study of high-affinity lactate handling in a colorectal cancer context. MCT2 has higher affinity for lactate than MCT1/MCT4 (Km ~0.7 mM vs ~5 mM and ~30 mM respectively) — making it particularly relevant in tissues where physiological lactate concentrations are low. Rescue with wild-type or transport-deficient MCT2 enables structure-function studies. Note that MCT2 requires embigin (EMB), not basigin (CD147), as its ancillary protein.

Primary applications: • High-affinity monocarboxylate uptake: ³H-lactate, ³H-pyruvate uptake at low substrate concentrations to characterize MCT2 high-affinity transport. • Embigin (EMB) ancillary protein studies: co-immunoprecipitation and trafficking analysis given MCT2's dependence on embigin rather than basigin. • MCT family comparison: parallel analysis with MCT1 (SLC16A1) and MCT4 (SLC16A3) for paralog-specific functions in cancer metabolism. • MCT inhibitor specificity: critical genetic control for AZD3965 (MCT1-selective) and other MCT-targeting compounds. EDITGENE recommends this model for researchers investigating monocarboxylate transport, cancer lactate handling, and MCT-targeted pharmacology.

Yes. MCT2 rescue experiments require attention to embigin partnership: • Construct design: use a codon-modified SLC16A7 sequence with a small C-terminal tag (FLAG, HA). MCT2 has 12 transmembrane domains. • Embigin partnership: MCT2 requires embigin (EMB), not basigin (CD147), for surface trafficking — confirm embigin expression in rescue cells or co-express embigin for full activity. • Transport-deficient rescue: substrate-binding pocket mutations enable structure-function studies. • Functional readout: rescue should restore high-affinity monocarboxylate uptake at low substrate concentrations (where MCT2 dominates over MCT1). HCT 116 transduces efficiently with lentivirus and supports stable rescue line generation.