ArticleNature communications2025
Deep learning prioritizes cancer mutations that alter protein nucleocytoplasmic shuttling to drive tumorigenesis.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed.
- Harnessing Deep Learning Models for Guide RNA Optimization and Off-Target Prediction in CRISPR Systems.Biotechnology journal · 2026Review
- Biology of PEST-containing nuclear proteins as potential targets in ovarian cancer (Review).Oncology letters · 2026Review
- MARCO+ Tumor-Associated Macrophages Impede CD8+ T Cell Immunity to Facilitate Immunotherapy Resistance in Renal Cell Carcinoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Deep learning prioritizes cancer mutations that alter protein nucleocytoplasmic shuttling to drive tumorigenesis.Nature communications · 2025Article
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Authors and funding
14 authors.
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Abstract
Genetic variants can affect protein function by driving aberrant subcellular localization. However, comprehensive analysis of how mutations promote tumor progression by influencing nuclear localization is currently lacking. Here, we systematically characterize potential shuttling-attacking mutations (SAMs) across cancers through developing the deep learning model pSAM for the ab initio decoding of the sequence determinants of nucleocytoplasmic shuttling. Leveraging cancer mutations across 11 cancer types, we find that SAMs enrich functional genetic variations and critical genes in cancer. We experimentally validate a dozen SAMs, among which R14M in PTEN, P255L in CHFR, etc. are identified to disrupt the nuclear localization signals through interfering their interactions with importins. Further studies confirm that the nucleocytoplasmic shuttling altered by SAMs in PTEN and CHFR rewire the downstream signaling and eliminate their function of tumor suppression. Thus, this study will help to understand the molecular traits of nucleocytoplasmic shuttling and their dysfunctions mediated by genetic variants.
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