The GSDMC Knockout MCF-7 Polyclonal Cells product provides a CRISPR/Cas9-edited polyclonal knockout cell population targeting the GSDMC gene in the MCF-7 human breast adenocarcinoma epithelial cell line. This polyclonal knockout cell resource is designed for studying the functional consequences of GSDMC disruption in a well-established model of luminal A breast cancer. The heterogeneous population reflects the diversity of editing outcomes generated by CRISPR/Cas9-mediated gene disruption, enabling robust assessment of phenotype?Cgenotype relationships in pooled knockout cells. It is suitable for loss-of-function experiments investigating the role of GSDMC in pyroptotic cell death, inflammatory signaling, and tumor biology.
The MCF-7 host cell line originates from a metastatic pleural effusion of a breast adenocarcinoma patient and is characterized as estrogen receptor (ER)-positive, progesterone receptor (PR)-positive, and human epidermal growth factor receptor 2 (HER2)-negative. These molecular features classify MCF-7 as a representative model for luminal A breast cancer, the most common clinical breast cancer subtype. The cells retain epithelial morphology and key signaling pathways relevant to hormone-dependent growth and survival, making them a broadly used platform for dissecting oncogenic mechanisms, drug responsiveness, and cell death pathways in breast cancer research.
GSDMC encodes a member of the gasdermin family of pore-forming proteins that act as executioners of pyroptosis, a lytic and inflammatory form of programmed cell death. The full-length GSDMC protein is maintained in an autoinhibited state until proteolytic cleavage by caspase-8, often activated downstream of tumor necrosis factor (TNF) receptor engagement under specific conditions. This cleavage liberates the N-terminal fragment, which oligomerizes and inserts into the plasma membrane to create pores, leading to cell swelling, membrane rupture, and release of pro-inflammatory cytokines such as interleukin-1?? (IL-1??) and IL-18. GSDMC expression is transcriptionally regulated by the tumor suppressor p53, linking DNA damage responses and cellular stress to pyroptotic death. GSDMC functionally interacts with other gasdermins, notably GSDMD, and participates in a signaling cascade involving TNF receptor, caspase-8, and the N-terminal pore-forming domain.
In the MCF-7 luminal A breast cancer context, GSDMC knockout provides a valuable tool to disentangle the contributions of pyroptosis to tumor cell fate and the immune microenvironment. Given the ER+/PR+/HER2? status and p53-mediated transcriptional control of GSDMC, this model allows researchers to examine how inflammatory cell death is regulated in hormone-responsive breast cancer cells. Disruption of GSDMC may reveal effects on cell survival, cytokine secretion profiles, and sensitivity to chemotherapeutic agents that induce pyroptosis. Because MCF-7 cells express functional p53, the knockout model is particularly useful for studying p53-dependent pyroptotic pathways and their cross-talk with apoptosis and necroptosis in breast adenocarcinoma.
This polyclonal knockout cell population supports a wide range of experimental applications, including analysis of pyroptotic signaling by western blotting for GSDMC and cleaved caspase-8, quantification of cell death via lactate dehydrogenase (LDH) release or flow cytometry with annexin V/propidium iodide staining, and measurement of IL-1?? and IL-18 release by ELISA. Researchers can also evaluate the transcriptional regulation of downstream p53 target genes using RT-qPCR and investigate migratory and invasive properties of the cells. The knockout model is suitable for drug sensitivity screens aimed at identifying compounds that induce pyroptosis in ER+ breast cancer, as well as for studying the interplay between inflammatory cell death and tumor microenvironment remodeling. For additional technical details or to discuss your specific experimental needs, please contact Ascent Research.
