The HSF1 Knockout HGC-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HGC-27 human gastric adenocarcinoma cell line, featuring targeted disruption of the HSF1 gene. This loss-of-function model enables researchers to investigate HSF1-dependent biological processes in a clinically relevant gastric cancer context. The polyclonal format provides a heterogeneous knockout pool suitable for functional genomics studies, drug target validation, and phenotypic screening.
HGC-27 is a poorly differentiated gastric adenocarcinoma cell line originally established from a lymph node metastasis of a 69-year-old female patient. The cells are tumorigenic in nude mice and exhibit epithelial characteristics, making them a widely used model for gastric cancer research. Their aggressive phenotype and metastatic origin recapitulate key aspects of advanced gastric malignancy, providing a robust cellular background for studying oncogenic signaling and therapeutic responses.
HSF1 serves as the master transcriptional regulator of the heat shock response, directing cellular adaptation to proteotoxic stress. Upon activation by stimuli such as heat shock, oxidative stress, or proteasome inhibition, HSF1 trimerizes, binds heat shock elements, and drives expression of molecular chaperones including HSP70, HSP90, HSP27, BAG3, and CHIP to restore protein homeostasis. In cancer, HSF1 is phosphorylated by kinases such as mTOR, AKT, ERK, PLK1, CK2, and GSK3, leading to its constitutive activity that supports oncogenic proliferation. It interacts with HSP90, HSP70, BAG3, CHIP, HSBP1, mTOR, and p53, integrating stress signals with growth and survival pathways.
In HGC-27 gastric cancer cells, HSF1 is expected to play a critical role in sustaining the malignant phenotype, as high HSF1 activity is frequently associated with tumor progression and therapeutic resistance. Disruption of HSF1 in this model permits dissection of its contribution to proteotoxic stress management, proliferation, and survival specifically within a gastric adenocarcinoma context. The polyclonal knockout population allows for the study of heterogeneous loss-of-function effects, avoiding clonal biases and better reflecting the complexity of cancer cell populations.
This polyclonal knockout model is suited for cancer biology and stress response research, including HSF1 target validation, inhibitor screening, and proteostasis network analysis. Relevant assays encompass Western blotting for HSF1 and downstream targets like HSP70, RT-qPCR for heat shock genes, immunofluorescence localization, and HSF1-luciferase reporter assays. Functional studies such as apoptosis, migration/invasion, and drug sensitivity testing with HSP90 inhibitors further extend its utility. For further information, contact Ascent Research.
