The NBR1 Knockout KYSE-150 Cell Line is a genetically engineered human cell model featuring CRISPR/Cas9-mediated disruption of the NBR1 gene. This knockout cell line provides a targeted loss-of-function platform for dissecting the roles of NBR1 in selective autophagy processes. By eliminating endogenous NBR1 expression, the model enables precise investigation of cargo recognition, aggregate clearance, and related signaling cascades in a controlled in vitro system. The product is delivered as a ready-to-use cell line suitable for functional assays in cancer biology and autophagy research.
The parental KYSE-150 cell line is a well-established human esophageal squamous cell carcinoma (ESCC) model derived from an epithelial origin. KYSE-150 cells exhibit characteristic features of esophageal cancer, including dysregulated growth signaling and invasive properties, making them a relevant host for studying oncogenic mechanisms and therapeutic vulnerabilities. This epithelial cell background provides a physiologically pertinent context for examining the interplay between autophagy and cancer progression, particularly in esophageal malignancies.
NBR1 functions as a pivotal autophagy cargo receptor, mediating the selective degradation of ubiquitinated substrates. It interacts with ubiquitinated protein aggregates and damaged organelles via its UBA domain, while its LIR motif engages autophagosomal LC3/GABARAP proteins to direct cargo for lysosomal destruction. NBR1 cooperates with p62/SQSTM1 and ATG8 family members, integrating signals from upstream regulators such as TFEB and mTORC1. Downstream, it targets ubiquitinated protein aggregates and peroxisomes, linking it to aggrephagy, pexophagy, and mTOR signaling pathway modulation. The protein also interacts with TAX1BP1, further expanding its network in cargo sorting and clearance.
In esophageal squamous cell carcinoma, NBR1-mediated autophagy is implicated in tumor cell homeostasis, stress adaptation, and resistance to therapeutic agents. Loss of NBR1 in the KYSE-150 background allows dissection of its contribution to oncogenic processes, including proliferation, migration, and drug sensitivity. Given the role of autophagy in cancer cell survival under nutrient deprivation and hypoxic conditions, this knockout model is valuable for probing the molecular determinants of resilience in esophageal cancer cells.
Representative research applications include monitoring autophagic flux with bafilomycin A1 treatment, evaluating LC3 puncta formation by immunofluorescence, assessing NBR1-LC3 interactions via co-immunoprecipitation, and quantifying cell proliferation through MTT or CCK-8 assays. The model also supports wound healing migration assays and drug sensitivity profiling to explore chemoresistance mechanisms. Collectively, these tools empower investigations into autophagy-dependent cancer pathways. For further details and batch-specific data, please contact Ascent Research.
