HSF1 Knockout KYSE-150 Polyclonal Cells constitute a CRISPR/Cas9-engineered polyclonal knockout cell population generated from the human esophageal squamous cell carcinoma line KYSE-150, with targeted disruption of the HSF1 gene. This polyclonal format avoids single-cell cloning bottlenecks and preserves cellular heterogeneity, providing a robust model for loss-of-function studies. The knockout pool is suitable for immediate culture expansion and downstream applications in stress biology and oncology research.
KYSE-150 is a well-characterized cell line derived from a Japanese patient with esophageal squamous cell carcinoma. These cells exhibit epithelial morphology and invasive potential, making them a standard model for studying ESCC pathogenesis, invasion, and therapeutic responses. The genetic background of KYSE-150, combined with its tumorigenic properties, offers a clinically relevant platform to interrogate molecular mechanisms underlying cancer cell survival and drug resistance.
HSF1 functions as the master transcriptional regulator of the heat shock response, orchestrating the expression of molecular chaperones including HSP70 (HSPA1A), HSP90 (HSP90AA1), and HSP27 (HSPB1). Its activity is modulated by upstream stress signals such as mTORC1, AMPK, and SIRT1, and involves trimerization, phosphorylation at Ser326, and nuclear translocation to bind heat shock elements (HSEs) in target gene promoters. HSF1 also interacts with co-regulators like HSP90, HSP70, HSBP1, DAXX, and eEF1A, and transcriptionally controls anti-apoptotic factors such as BCL2L1 and cochaperone BAG3, thereby integrating proteotoxic stress responses with cell survival pathways.
Disruption of HSF1 in KYSE-150 abrogates the cellular heat shock response, impairing the ability to maintain proteostasis under stressful conditions typical of the tumor microenvironment. Given the reliance of cancer cells on chaperone networks for survival, HSF1 knockout sensitizes ESCC cells to proteotoxic insults, potentially revealing vulnerabilities in stress adaptation and drug resistance mechanisms. This model enables dissection of HSF1-dependent signaling in a relevant epithelial cancer background.
This knockout model supports a broad range of functional assays, including western blotting to assess HSF1 and downstream effector expression, RT-qPCR for heat shock gene induction, ChIP-qPCR to measure HSF1 occupancy at HSEs, and luciferase reporter assays for transcriptional activity. Cell viability and apoptosis assays under heat shock or chemotherapeutic stress allow evaluation of stress sensitivity. For further information and technical support, please contact Ascent Research.
