The LINC01140 Knockout AC16 Cell Line is a CRISPR/Cas9-edited knockout cell line featuring a targeted disruption of the long non-coding RNA LINC01140 gene in the AC16 human ventricular cardiomyocyte cell line. This loss-of-function model provides a robust platform for investigating the regulatory roles of LINC01140 in cardiomyocyte biology, particularly in the context of cardiac stress and disease. The cell line is designed to enable precise delineation of LINC01140-dependent molecular mechanisms without the interference of endogenous gene expression, making it an essential tool for functional genomics and pathway analysis in cardiovascular research.
The AC16 host cell line is an immortalized human adult ventricular cardiomyocyte line that faithfully retains key characteristics of primary cardiomyocytes, including contractile function, electrophysiological activity, and metabolic homeostasis. These cells express cardiac-specific markers and maintain the structural and signaling machinery critical for cardiac muscle physiology. Their ventricular origin and stable phenotype render them highly suitable for modeling human cardiac diseases and for screening cardioprotective compounds, providing a physiologically relevant background for knockout studies.
LINC01140 acts as a competitive endogenous RNA (ceRNA) that sponges miR-23a-3p, leading to upregulation of PTEN and subsequent inhibition of AKT signaling. This mechanism promotes cardiomyocyte apoptosis while suppressing proliferation and hypertrophic growth. Additionally, LINC01140 interacts with EZH2 and SUZ12, core components of the polycomb repressive complex 2 (PRC2), to epigenetically silence pro-survival genes. Its expression is activated by upstream regulators such as HIF1A, NFKB1, and TGFB1, and it modulates downstream effectors including BCL2, BAX, and CCND1, thereby integrating into the PI3K/AKT, Wnt/??-catenin, MAPK/ERK, and Hippo signaling pathways.
In the AC16 cardiomyocyte context, LINC01140 knockout enables dissection of its roles in apoptosis, proliferation, and hypertrophy under basal and stress conditions. This model is particularly relevant for studying ischemia-reperfusion injury, cardiac hypertrophy, myocardial infarction, and heart failure, where LINC01140-mediated signaling contributes to pathological remodeling. By eliminating LINC01140, researchers can assess its impact on cell viability, mitochondrial function, and contractile properties, offering insights into potential therapeutic targets for cardioprotection.
This knockout cell line is suited for a wide range of experimental applications, including mechanistic studies of lncRNAs in cardiac pathology, high-content screening for cardioprotective drugs, and functional genomics analyses. Representative assays include RT-qPCR and western blotting for expression profiling, RNA-seq for transcriptome-wide effects, luciferase reporter assays for miRNA interaction validation, and apoptosis assays such as TUNEL. Additional techniques like RNA immunoprecipitation (RIP), chromatin isolation by RNA purification (ChIRP), and cardiomyocyte hypertrophy measurements further expand its utility. For more information or to discuss your research needs, please contact Ascent Research.
