In Stock Cell Lines
Homo sapiens (Human)
Large intestine (colon)
Adherent
The SLC22A15 Knockout HCT 116 Cell Line is a CRISPR/Cas9-edited knockout human colorectal carcinoma cell line. It features targeted gene disruption of SLC22A15, which encodes a putative organic cation transporter in the SLC22 solute carrier family. The HCT 116 host cell line is characterized by microsatellite instability, reflecting a clinically relevant colorectal cancer subtype. This loss-of-function model enables investigation of SLC22A15 in drug transport, chemosensitivity, and metabolite handling within a colorectal cancer context. Key applications include drug sensitivity assays, transportome profiling, and intracellular metabolite analysis, making it ideal for functional characterization and pharmacological studies.
FMR1 Knockout TE1 Polyclonal Cells
Cat. No. ARG12209
IFI16 Knockout NCI-H1975 Polyclonal Cells
Cat. No. ARG31697
BBX Knockout jurkat Polyclonal Cells
Cat. No. ARG33986
DRAM2 Knockout K562 Polyclonal Cells
Cat. No. ARG39769
ISOC1 Knockout huh-7 Polyclonal Cells
Cat. No. ARG28415
NUCKS1 Knockout 786-O Polyclonal Cells
Cat. No. ARG5684
The SLC22A15 Knockout HCT 116 Cell Line is a CRISPR/Cas9-edited knockout cell line with targeted disruption of the SLC22A15 gene. This model abolishes expression of solute carrier family 22 member 15, a putative organic cation transporter. The gene editing ensures stable ablation of SLC22A15, providing a clean loss-of-function system for functional studies. It is validated for knockout efficiency and ready for downstream assays.
HCT 116 is a human colorectal carcinoma cell line with epithelial morphology and microsatellite instability (MSI) arising from MLH1 deficiency. This widely used model recapitulates key features of colorectal cancer, including altered drug metabolism and transport pathways. The MSI background makes HCT 116 particularly relevant for studying chemosensitivity and resistance mechanisms. The SLC22A15 knockout derivative thus combines a well-characterized cancer background with a defined genetic modification for transporter research.
SLC22A15 encodes a member of the SLC22 solute carrier family, predicted to mediate transport of organic cations across cell membranes. Its function likely influences intracellular concentrations of diverse endogenous and exogenous cations. The precise regulatory mechanisms and interacting partners remain undefined. Knockout of SLC22A15 eliminates this predicted transport activity, potentially altering drug and metabolite distribution. Downstream effects may impact cation-dependent signaling or cellular responses, though specific molecular targets are uncharacterized.
In HCT 116 cells, SLC22A15 knockout enables dissection of transporter contributions to colorectal cancer biology. The model is valuable for assessing whether SLC22A15 affects sensitivity to chemotherapeutics like oxaliplatin or 5-fluorouracil, or modulates metabolite levels relevant to tumor progression. The MSI context further allows examination of transporter?CDNA repair interplay. This system can reveal roles of organic cation transport in drug resistance or toxicity within a colorectal cancer framework.
Typical applications include drug transport assays with radiolabeled substrates, drug sensitivity profiling (e.g., MTT assays), and transportome analysis. Knockout validation by RT-qPCR or western blot confirms gene disruption. Intracellular metabolite profiling via mass spectrometry defines changes in organic cation pools. RNA-seq can uncover transcriptomic adaptations. These approaches support comprehensive SLC22A15 characterization. For further information, contact Ascent Research.
