ArticleNature communications2024
Targeting ERK-MYD88 interaction leads to ERK dysregulation and immunogenic cancer cell death.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- The circMTCL1/miR-145-5p/BMP3 axis suppresses colorectal cancer cell growth by mediating the MAPK signaling pathway.Medical oncology (Northwood, London, England) · 2026Article
- Nilotinib induces immunogenic cuproptosis to potentiate cancer immunotherapy.Cell reports. Medicine · 2026Article
- Non-canonical signaling hubs upon inhibition of MyD88-ERK interaction in cancer.Cell death & disease · 2026Article
- The integrated stress response in cancer: mechanisms of tumor adaptation and therapeutic targeting.Biochemical Society transactions · 2026Review
- A small molecule targets LIC1 to suppress lung tumor growth by inducing autophagy.Nature chemical biology · 2026Article
- TMEM121 suppresses cervical cancer cell proliferation and migration via interaction with the ERK pathway.American journal of cancer research · 2026Article
Corrections and comments
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Authors and funding
25 authors.
Funding
Abstract
The quest for targeted therapies is critical in the battle against cancer. The RAS/MAP kinase pathway is frequently implicated in neoplasia, with ERK playing a crucial role as the most distal kinase in the RAS signaling cascade. Our previous research demonstrated that the interaction between ERK and MYD88, an adaptor protein in innate immunity, is crucial for RAS-dependent transformation and cancer cell survival. In this study, we examine the biological consequences of disrupting the ERK-MYD88 interaction through the ERK D-recruitment site (DRS), while preserving ERK's kinase activity. Our results indicate that EI-52, a small-molecule benzimidazole targeting ERK-MYD88 interaction induces an HRI-mediated integrated stress response (ISR), resulting in immunogenic apoptosis specific to cancer cells. Additionally, EI-52 exhibits anti-tumor efficacy in patient-derived tumors and induces an anti-tumor T cell response in mice in vivo. These findings suggest that inhibiting the ERK-MYD88 interaction may be a promising therapeutic approach in cancer treatment.
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