ArticleGenes & genomics2025
Effects of Zonula occludens-1 (ZO-1) tight junction protein on tumor characteristics in human ovarian cancer cells.
Article in Genes & genomics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Transcriptomic analysis of zonula occludens-1 (ZO-1) knockout in ovarian cancer cell lines.Genes & genomics · 2026Article
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Authors and funding
12 authors.
Funding
Abstract
backgroundOvarian cancer is among the most lethal malignancies affecting women, largely due to its asymptomatic progression in early stages, rapid advancement, and high mortality rate. Tight junction protein 1 (TJP1), also known as Zonula occludens-1 (ZO-1), plays a critical role in epithelial and endothelial cell integrity by regulating paracellular permeability. Additionally, ZO-1 is involved in cell-cell communication networks, influencing cellular proliferation, differentiation, and metastasis. While previous studies have demonstrated the significance of ZO-1 in tumorigenesis and cancer progression, its precise mechanistic role remains to be fully elucidated.
objectiveThis study aims to investigate the functional role of ZO-1 in human ovarian cancer cells to provide a molecular perspective on its impact on tumor progression.
methodsHuman ovarian cancer cell lines SNU119 and SKOV3 were utilized. ZO-1 knockout (KO) was achieved using the Clustered Regularly Interspaced Short Palindromic Repeats-CRISPR-associated protein 9 (CRISPR-Cas9) system in combination with single-guide RNA (sgRNA) targeting ZO-1. Hygromycin B selection was employed to establish stable ZO-1 KO SNU119 and ZO-1 KO SKOV3 cell lines. The successful knockout of ZO-1 was confirmed at both the transcript and protein levels via real-time quantitative PCR (RT-qPCR) and Western blotting. Functional assays, including cell proliferation, migration, and invasion assays, were conducted to assess the effects of ZO-1 KO on key tumor-associated characteristics.
resultsCRISPR-Cas9-mediated ZO-1 KO in SNU119 and SKOV3 ovarian cancer cell lines resulted in a significant reduction of ZO-1 expression at both the transcript and protein levels. The loss of ZO-1 led to a disruption of cell-cell junctions. Functionally, ZO-1 KO cells exhibited reduced proliferation, whereas cell migration and invasion were significantly enhanced, suggesting a shift toward a more aggressive phenotype.
conclusionThe findings indicate that ZO-1 KO in ovarian cancer cells suppresses cell proliferation while promoting migratory and invasive properties, hallmarks of tumor progression. These results underscore the complex role of ZO-1 in ovarian cancer and highlight the need for further investigation into its broader regulatory impact on oncogenic pathways.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.