In Stock Cell Lines
Homo sapiens (Human)
Large intestine (colon)
Adherent
The SLC22A15 Knockout HT-29 Cell Line is a CRISPR/Cas9-edited knockout cell line derived from HT-29 colorectal adenocarcinoma cells. It provides a loss-of-function model targeting SLC22A15, an organic cation and L-carnitine transporter, thereby disrupting carnitine homeostasis and fatty acid ??-oxidation. Regulated by PPAR?? and FXR and interacting with PDZK1, SLC22A15 influences downstream effectors such as CPT1A and ACADM. This model is designed for cancer metabolism research, including metabolomic profiling, drug transport studies, metabolic flux analyses, and drug sensitivity assays.
KIT Knockout A549 Polyclonal Cells
Cat. No. ARG23124
GOLM1 Knockout HT29 Polyclonal Cells
Cat. No. ARG33254
HSPB1 Knockout HEK293T Polyclonal Cells
Cat. No. ARG37990
CARHSP1 Knockout K562 Polyclonal Cells
Cat. No. ARG42325
CPB1 Knockout HCT116 Polyclonal Cells
Cat. No. ARG7048
LAPC-4
Cat. No. ARC0435
The SLC22A15 Knockout HT-29 Cell Line is a CRISPR/Cas9-edited knockout cell line derived from HT-29 human colorectal adenocarcinoma cells. It provides a targeted loss-of-function model for SLC22A15, which encodes an organic cation/L-carnitine transporter. The cell line is generated via CRISPR/Cas9-mediated gene disruption and supplied as a validated knockout population for studies in cancer metabolism and transporter biology.
HT-29 cells, established from a primary human colorectal adenocarcinoma, display adherent epithelial morphology and retain key intestinal epithelial properties, including the capacity to differentiate. This cell line is widely employed as a model for intestinal epithelial biology, colorectal cancer research, and studies of transport and tumorigenesis, making it a suitable host for examining SLC22A15 function in colon cancer metabolism.
SLC22A15 functions as a plasma membrane transporter mediating the uptake of L-carnitine and organic cations, critical for mitochondrial fatty acid ??-oxidation. Its expression is transcriptionally regulated by PPAR??, FXR, and PGC-1??, and it interacts with the scaffolding protein PDZK1. Downstream, imported carnitine supports the acylcarnitine shuttle involving CPT1 and CPT2, which transports fatty acids into mitochondria for oxidation by enzymes such as ACADM. Given the role of carnitine in shuttling long-chain fatty acids, SLC22A15 knockout may blunt fatty acid oxidation and force metabolic adaptation, potentially sensitizing cells to metabolic stress. Disruption of SLC22A15 in HT-29 cells is therefore expected to disturb carnitine homeostasis, impair mitochondrial fatty acid oxidation, and alter metabolic pathways relevant to colorectal cancer cell proliferation.
In HT-29 colorectal adenocarcinoma cells, SLC22A15 knockout provides a physiologically relevant system to dissect the contribution of carnitine-dependent metabolism to tumor cell growth. Colorectal cancers frequently exhibit metabolic reprogramming, including altered fatty acid oxidation, which is increasingly recognized as a therapeutic vulnerability. By eliminating SLC22A15 function, researchers can evaluate its impact on mitochondrial respiration, cellular energy status, and sensitivity to metabolic inhibitors, thereby uncovering metabolic liabilities and potential drug targets in colorectal cancer.
This knockout cell line is ideally suited for a broad range of experimental applications, including metabolomic profiling, drug transporter studies, and cancer metabolism research. Functional assays such as L-carnitine uptake measurements, fatty acid oxidation assays, and Seahorse metabolic flux analyses enable detailed characterization of metabolic reprogramming. Additionally, RT-qPCR and Western blotting confirm target gene disruption, while cell viability (MTT) and proliferation assays assess growth phenotypes. The SLC22A15 Knockout HT-29 Cell Line supports functional genomics and drug sensitivity screens aimed at identifying metabolic dependencies in colorectal cancer. For further information, please contact Ascent Research.
