The IL11 Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HeLa human cervical adenocarcinoma line. This product provides a loss-of-function model for interleukin-11, a pleiotropic cytokine of the IL-6 family, generated through CRISPR/Cas9-mediated gene disruption. The polyclonal format ensures a heterogeneous knockout population that reflects the genetic diversity of the edited pool, suitable for robust functional studies without clonal selection artifacts.
The parental HeLa cell line is an HPV18-positive, adherent epithelial model widely used in cancer research. Its tumorigenic properties stem from p53 degradation by HPV18 E6, active telomerase, and transformed metabolism. As a cervical cancer model, HeLa cells offer a tractable system for investigating oncogenic signaling, drug responses, and metastasis-related phenotypes in vitro.
IL11 signals via a heterodimeric receptor complex of IL11RA and gp130 (IL6ST), triggering phosphorylation of JAK1/JAK2 and downstream activation of STAT3, MAPK/ERK, and PI3K/AKT pathways. Upstream regulators include TGF-??, IL-1, TNF-??, hypoxia, and AP-1. Activated STAT3 translocates to the nucleus, promoting transcription of target genes such as BCL2, BCLXL, Cyclin D1, MMP9, VEGFA, and Survivin, which collectively drive proliferation, survival, and migration. Negative feedback is mediated by SOCS3, an interacting factor that dampens JAK/STAT signaling.
In HeLa cells, IL11 contributes to oncogenic processes. Dysregulated IL11 expression can foster epithelial?Cmesenchymal transition, invasion, and resistance to apoptosis, partly through STAT3-mediated transcriptional programs. This knockout model enables dissection of IL11-dependent signaling in a cervical cancer context where HPV-driven transformation and JAK/STAT crosstalk are pivotal. It is particularly relevant for studying how the tumor microenvironment and stromal cues, such as TGF-??, converge on IL11 to promote malignant progression.
Typical applications include profiling STAT3 phosphorylation by western blot, monitoring proliferation via MTT assay, assessing migratory capacity in wound healing and transwell invasion assays, and quantifying apoptosis by flow cytometry. This model is also employed for RT-qPCR analysis of IL11-responsive genes, colony formation assays, secretome analysis by ELISA, and transcriptomic profiling via RNA-seq. The polyclonal IL11 knockout HeLa cells support functional interrogation of IL11 in cancer signaling, anti-fibrotic screening, and investigation of JAK-STAT-driven drug resistance. For further details, contact Ascent Research.
