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CRISPR-Induced Loss of Connexin 43 Expression Sensitizes KRAS Mutant Cells to Cisplatin
Gap Junction intercellular communication (GJIC) is often dysregulated in cancers, and this dysregulation has been shown to have pro-tumorigenic effects. Connexins (Cxs) are transmembrane proteins that make up gap junctions. Previous studies have indicated that RNA interference (RNAi)-based suppressi...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Caltech Library
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9701319/ https://www.ncbi.nlm.nih.gov/pubmed/36447529 http://dx.doi.org/10.17912/micropub.biology.000681 |
Sumario: | Gap Junction intercellular communication (GJIC) is often dysregulated in cancers, and this dysregulation has been shown to have pro-tumorigenic effects. Connexins (Cxs) are transmembrane proteins that make up gap junctions. Previous studies have indicated that RNA interference (RNAi)-based suppression of Cx43 increases cellular resistance to the chemotherapeutic agent cisplatin. Interestingly, we found that the loss of Cx43 expression induced by the CRISPR-Cas9 technology sensitizes cells to cisplatin in a KRAS mutant-dependent manner. |
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