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CRISPR/Cas9-Mediated PTPRZ1 Knockout Suppresses LUSC Proliferation with Genome-Wide Off-Target Analysis

ABSTRACT: To investigate the potential role of the PTPRZ1 in tumor development, we leveraged CRISPR/Cas9 to perform knockout experiments in two distinct LUSC cell lines, H520 and HCC95, both characterized by high cellular expression of the gene. Following the disruption of PTPRZ1, we observed a significant reduction in the proliferation of both LUSC cell lines, as indicated by the Cell Counting Kit-8 (CCK-8) assay .To comprehensively assess potential off-target effects of the CRISPR/Cas9 editing, we conducted whole-genome sequencing comparing the HCC95-NC and HCC95-KO-PTPRZ1cell lines, which enabled genome-wide evaluation of editing specificity

ORGANISM(S): Homo sapiens

PROVIDER: GSE306332 | GEO | 2025/09/02

REPOSITORIES: GEO

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Project description:Lung squamous cell carcinoma (LUSC) is associated with poor survival owing to the lack of advanced targeted therapies, due to the incomplete characterization of complex genetic profiles. Therefore, it is essential to elucidate the molecular mechanisms of LUSC via the mice model and human database to understand the LUSC pathogenesis. A LUSC BALB/c mice model was established using N-nitroso-tris-chloroethylurea (NTCU). After termination of mice, the lung tissues were subjected to RNA sequencing. First, DESeq2 was used to normalize the read count, followed by gene set enrichment analysis (GSEA) to identify the affected pathways in LUSC. Subsequently, the pathogenic single nucleotide polymorphism (SNP) was determined using Protein Variation Effect Analyzer (PROVEAN) and Sorting Intolerant From Tolerant (SIFT), following scores of < 0.05 and < -2.5, respectively, which were then functionally enriched using g:Profiler. The transcriptomic profile of human LUSC patients was obtained from The International Cancer Genome Consortium (ICGC) and analyzed. The impact of pathogenic simple somatic mutation in human LUSC was determined using the Combined Annotation Dependent Depletion (CADD) score, which was functionally enriched using g:Profiler. Additionally, the enriched pathway of LUSC patients with complete remission (responsive) was compared with those with disease progression or deceased (non-responsive) post-GSEA treatment. All pathway analysis was possibly referred to the Reactome database, and an adjusted p-value < 0.05 was considered statistically significant. Based on the transcriptomic analysis of LUSC mice, the top pathway enriched from the animal study and human LUSC revealed similarity in four major themes: cholesterol, cellular interaction, immune, and extracellular matrix dysregulation. Furthermore, the overrepresented pathways identified in LUSC patients were consistent with the four major themes dysregulated in LUSC tumors. This study identified several biological pathways that may contribute to LUSC development and potential targets for future LUSC therapy.

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CRISPR/Cas9-Mediated PTPRZ1 Knockout Suppresses LUSC Proliferation with Genome-Wide Off-Target Analysis

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