SLC2A11 Knockout Cell Line (HCT116)

The choice depends on whether you are studying SLC2A11 (GLUT11)'s role in cancer cell hexose metabolism, particularly relevant for fructose handling in colorectal cancer contexts. The Knockout line is appropriate for asking whether GLUT11 contributes to fructose or glucose uptake in colorectal cancer cells — GLUT11's fructose preference makes it relevant for cancer cell sugar metabolism studies. Overexpression is useful for studying isoform-specific functions or for testing cancer-associated GLUT11 effects. For colorectal cancer fructose metabolism research, the EDITGENE Knockout in HCT 116 is particularly relevant — fructose has emerging roles in colorectal cancer progression, and GLUT11 may contribute to fructose acquisition in this context. This product complements the parallel SLC2A11 Knockout in HEK293 (also available); HCT 116 is preferred for cancer biology studies and intestinal-derived contexts. Rescue with wild-type or transport-deficient GLUT11 enables structure-function studies.

Primary applications: • Cancer hexose metabolism: glucose and fructose uptake in the colorectal cancer context to assess GLUT11's contribution. • Fructose-driven proliferation: assessment of fructose as a carbon source for HCT 116 proliferation in the absence of GLUT11. • GLUT family expression analysis: characterization of GLUT1, GLUT3, GLUT5 compensatory expression in GLUT11-null colorectal cancer cells. • CRC fructose biology: emerging research connects dietary fructose to colorectal cancer progression — GLUT11 KO enables direct testing of this hypothesis. EDITGENE recommends this HCT 116-based model for colorectal cancer fructose metabolism research; the parallel SLC2A11 Knockout in HEK293 is preferred for biochemical mechanism studies.

Yes. GLUT11 rescue in HCT 116 is well-suited for cancer biology research: • Construct design: use a codon-modified SLC2A11 sequence with a small C-terminal tag (FLAG, HA). Both N- and C-terminal cytoplasmic tags are typically tolerated. • Cancer phenotype rescue: assessment of proliferation, anchorage-independent growth, and fructose utilization restoration following GLUT11 rescue. • Transport-deficient rescue: substrate-binding pocket mutations enable distinguishing transport activity from non-transport functions in cancer biology. • Functional readout: rescue should restore fructose and glucose uptake activities and colorectal cancer-relevant metabolic phenotypes. HCT 116 transduces efficiently with lentivirus and supports stable rescue line generation.