ArticleCell death & disease2024
YY1 downregulation underlies therapeutic response to molecular targeted agents.
Article in Cell death & disease, 2024. 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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Who cites it
4 citing papers in PubMed.
- Mutations in untranslated non-coding regions of EGFR, AKT1 & HRAS modulate their expression regulatory networks to facilitate progression of colorectal cancer.Functional & integrative genomics · 2026Article
- CXCR4, CXCR7 and PBRM1 are responsible for everolimus and cabozantinib resistance in human renal cancer cells.Cell death discovery · 2026Article
- Targeting tumor transition windows.Exploration of targeted anti-tumor therapy · 2026Review
- DAGFormer: A graph-based domain adaptation approach for single-cell cancer drug response prediction.PLoS computational biology · 2025Article
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Authors and funding
19 authors.
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Abstract
During targeted treatment, oncogene-addicted tumor cells often evolve from an initial drug-sensitive state through a drug-tolerant persister bottleneck toward the ultimate emergence of drug-resistant clones. The molecular basis underlying this therapy-induced evolutionary trajectory has not yet been completely elucidated. Here, we employed a multifaceted approach and implicated the convergent role of transcription factor Yin Yang 1 (YY1) in the course of diverse targeted kinase inhibitors. Specifically, pharmacological perturbation of the receptor tyrosine kinase (RTK)/mitogen-activated protein kinase (MAPK) pathway resulted in the downregulation of YY1 transcription, which subsequently resumed upon therapeutic escape. Failure to decrease YY1 subverted cytotoxic effects, whereas elimination of residual YY1 maximized anticancer efficacy and forestalled the emergence of drug resistance. Mechanistically, YY1 was uncovered to dictate cell cycle and autophagic programs. Immunohistochemical analysis on a wide spectrum of clinical specimens revealed that YY1 was ubiquitously expressed across lung adenocarcinomas and exhibited anticipated fluctuation in response to corresponding RTK/MAPK inhibition. These findings advance our understanding of targeted cancer management by highlighting YY1 as a determinant node in the context of genotype-directed agents.
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Registered trials
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