ArticleCancer cell international2024
Genome-wide CRISPR screen identifies ESPL1 limits the response of gastric cancer cells to apatinib.
Article in Cancer cell international, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- Lamin B1-dependent regulation of human separase in mitosis.Nucleic acids research · 2026Article
- Development and Validation of an Extra Spindle Pole Bodies-like 1-Based Diagnostic and Prognostic Model for Hepatitis B Virus-Related Hepatocellular Carcinoma: Retrospective Cohort Study.JMIR medical informatics · 2025Article
- CRISPR/Cas9 system: a novel approach to overcome chemotherapy and radiotherapy resistance in cancer.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- E2F1-mediatedCytoJournal · 2025Article
- Bioinformatics insights intoFrontiers in cell and developmental biology · 2025Article
- Expanding the CRISPR/Cas toolkit: applications in proteomics and theranostics.Frontiers in bioengineering and biotechnology · 2025Review
Corrections and comments
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Authors and funding
7 authors at 6 institutions in 1 country.
Funding
Abstract
Apatinib was the first anti-angiogenic agent approved for treatment of metastatic gastric cancer (GC). However, the emergence of resistance was inevitable. Thus investigating new and valuable off-target effect of apatinib directly against cancer cells is of great significance. Here, we identified extra spindle pole bodies-like 1 (ESPL1) was responsible for apatinib resistance in GC cells through CRISPR genome-wide gain-of-function screening. Loss of function studies further showed that ESPL1 inhibition suppressed cell proliferation, migration and promoted apoptosis in vitro, and accordingly ESPL1 knockdown sensitized GC cells to apatinib. In addition, we found ESPL1 interacted with mouse double minute 2 (MDM2), a E3 ubiquitin protein ligase, and the combination of MDM2 siRNA with apatinib synergistically ameliorated the resistance induced by ESPL1 overexpression. In summary, our study indicated that ESPL1 played a critical role in apatinib resistance in GC cells. Inhibition of MDM2 could rescue the sensitivity of GC cells to apatinib and reverse ESPL1-mediated resistance.
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Registered trials
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