What is the role of crosstalk between different post-translational modifications in lung cancer pathogenesis?
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Crosstalk between different post-translational modifications (PTMs) plays a crucial role in lung cancer pathogenesis. Studies have shown that proteins in lung cancer cells undergo various PTMs like phosphorylation, methylation, and acetylation, which collectively regulate cell signaling pathways. This intricate network of PTMs influences key cellular processes such as stem-like properties maintenance, gene expression control, and epithelial-mesenchymal transition in lung cancer cells. The interplay between PTMs can lead to the activation or inhibition of critical proteins involved in oncogenic signaling pathways, highlighting potential drug targets for combination therapies in lung cancer treatment. Understanding the crosstalk between different PTMs provides insights into the molecular mechanisms underlying lung cancer progression and offers avenues for developing targeted therapeutic approaches to combat this disease.
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35 Citations | Crosstalk between core fucosylation of E-cadherin and Src activation induces an epithelial-mesenchymal transition-like process in lung cancer cells, impacting migration and signaling pathways. |
| Crosstalk between post-translational modifications like phosphorylation and ubiquitination regulates oncogenic signaling pathways in lung cancer, influencing tumor progression and potential therapeutic targets. | |
18 Citations | The crosstalk between methylation and phosphorylation of LSH in lung cancer regulates stem-like properties, impacting cancer pathogenesis by influencing stemness and chemotherapy resistance. |
42 Citations | Crosstalk between phosphorylation, methylation, and acetylation in lung cancer integrates signaling pathways, revealing exclusive "OR" gates in signal transduction events and highlighting key proteins like EP300. |
| Crosstalk between post-translational modifications in lung cancer connects signaling pathways, revealing potential drug targets and synergistic therapy options, highlighting the interplay between cell signaling and metabolic reprogramming. |
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