Human PPARA Stable Cell Line - HCT 116

The PPARA gene encodes peroxisome proliferation-activating receptor α (PPARα), a member of the nuclear receptor superfamily of ligand-activated transcription factors. PPARα acts as a major metabolic sensor, coordinating gene expression involved in mitochondrial and peroxisome fatty acid β-oxidation, fatty acid transport, and ketone body synthesis. It is primarily expressed in tissues with high fatty acid catabolism rates, such as the liver, heart, and skeletal muscle. Activation of PPARα by endogenous ligands (e.g., long-chain fatty acids) or synthetic ligands (e.g., fibrates) leads to a systemic shift towards lipid utilization and increased insulin sensitivity. Clinically, PPARA is a major target for treating dyslipidemia and a focus of research in non-alcoholic steatohepatitis (NASH). In oncology, PPARα exerts anti-tumor effects in various cancers by inhibiting the Wahlberg effect and suppressing pro-inflammatory signaling. However, in human colorectal cancer, PPARA activity can promote the survival and drug resistance of tumor stem cells in hypoxic tumor core regions.

The HCT 116-based human PPARA-stable cell line provides an important model for studying the metabolic vulnerability of colorectal cancer and the potential of nuclear receptor-targeted therapy. HCT 116 is a highly proliferative human colon cancer cell line with well-defined genetic characteristics, making it a standard tool for exploring gastrointestinal oncology and drug response. By stably overexpressing human PPARA, researchers can investigate how activation of fatty acid oxidation pathways affects cancer cell growth, survival, and sensitivity to therapeutic stress. This product is invaluable for screening novel PPARA agonists or dual PPAR agonists for reprogramming the tumor metabolome or treating concurrent metabolic disorders. The PPARA-HCT 116 model enables detailed molecular analysis of how the PPAR signaling pathway interacts with the Wnt/β-catenin and NF-κB pathways to regulate tumor cell plasticity and the immune microenvironment.