The ING5 Knockout NCI-H1975 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population in which the ING5 gene has been disrupted, creating a loss-of-function model. This polyclonal format provides a heterogeneous pool of edited cells, enabling robust functional studies without clonal selection artifacts. The knockout abrogates ING5 expression, allowing interrogation of its tumor suppressor activities in a physiologically relevant lung adenocarcinoma background.
The NCI-H1975 parental line is a human non-small cell lung adenocarcinoma (NSCLC) cell line derived from the pleural effusion of a female patient. These epithelial cells harbor a KRAS mutation and retain wild-type EGFR, representing a clinically aggressive NSCLC subtype. NCI-H1975 is extensively used as a metastatic lung adenocarcinoma model, providing a relevant genetic context for studying oncogenic signaling and therapeutic resistance.
ING5 is a type II tumor suppressor that orchestrates chromatin remodeling, apoptosis, and cell cycle arrest through interactions with the p53 pathway. It forms complexes with p53, the acetyltransferase PCAF, and histone deacetylases HDAC1/2 within Sin3A corepressor assemblies, regulating histone H3 and H4 acetylation at target gene promoters. ING5 facilitates p53-mediated transactivation of CDKN1A (p21) and BAX while repressing CCND1. Loss of ING5 disrupts these complexes, impairing p53 stabilization and attenuating pro-apoptotic and cell cycle inhibitory gene expression, thus promoting survival and proliferation.
In NCI-H1975 cells, ING5 knockout eliminates a critical tumor suppressive barrier against KRAS-driven oncogenesis. The combination of ING5 loss and mutant KRAS generates a model that recapitulates hallmark features of aggressive NSCLC, including enhanced viability, apoptotic resistance, and aberrant chromatin acetylation. This polyclonal knockout population is therefore valuable for investigating epigenetic dysregulation mechanisms and screening compounds that may restore p53 function or induce synthetic lethality.
This product supports diverse research applications, including tumor suppressor mechanism studies, p53 pathway analysis, apoptosis research, and cancer drug resistance profiling. Assays such as Western blotting (ING5, p53, p21, Bax), RT-qPCR, MTT viability, annexin V apoptosis, cell cycle flow cytometry, ChIP-qPCR for histone acetylation, colony formation, and drug sensitivity screening are all applicable. The ING5 knockout polyclonal cells serve as a versatile tool for dissecting chromatin biology and lung adenocarcinoma modeling. For further details, please contact Ascent Research.
