The AMOTL1 Knockout A-549 Polyclonal Cells consist of a CRISPR/Cas9-edited polyclonal population with disrupted AMOTL1 gene expression in human A-549 lung adenocarcinoma cells. This heterogeneous pool, derived without single-cell cloning, provides a loss-of-function model that maintains genetic diversity, enabling robust functional studies while avoiding clonal artifacts.
The A-549 cell line originates from a 58-year-old male lung adenocarcinoma patient and exhibits an adherent epithelial morphology with a hypotriploid karyotype. These type II pneumocyte-like cells are a standard model for non-small cell lung cancer research, widely used for investigating oncogenic pathways, drug responses, and metastatic mechanisms.
AMOTL1 functions as a tight junction scaffold that critically regulates the Hippo pathway by recruiting MST1/2 and LATS1/2 kinases to junctional complexes. This scaffolding promotes phosphorylation and cytoplasmic retention of the transcriptional co-activators YAP and TAZ, inhibiting their nuclear interaction with TEAD factors and suppressing target genes like CTGF and CYR61. AMOTL1 also interacts with AMOT, AMOTL2, PALS1, PATJ, and RICH1 to maintain junctional integrity, and modulates RhoA signaling. Loss of AMOTL1 disrupts this network, leading to reduced LATS1/2 activity, YAP/TAZ nuclear translocation, and enhanced cell proliferation and migration.
In the A-549 lung adenocarcinoma background, AMOTL1 knockout mimics pathological Hippo pathway inactivation associated with tumor progression and metastasis. The disruption of junctional scaffolding amplifies YAP/TAZ-driven transcription and perturbs cell polarity, providing a relevant model to study molecular events that drive migration, invasion, and anchorage-independent growth in lung cancer cells.
These polyclonal knockout cells are designed for diverse applications including Hippo pathway analysis, YAP/TAZ target gene quantification by RT-qPCR, tight junction visualization via immunofluorescence (ZO-1, occludin), transwell migration/invasion assays, and TEAD luciferase reporter assays. Additional uses include co-immunoprecipitation for protein interaction studies and RNA-seq transcriptomics. This product supports both fundamental research and drug screening efforts targeting Hippo-YAP/TAZ signaling in lung cancer. For further information, contact Ascent Research.
