Loading
Life sciences · Journal article
Nature Communications · September 16, 2026
No summary has been generated for this record yet. What follows is drawn from its source metadata only.
Journal article.
No findings were extractable from the material analysed.
Safety was not reported in the material analysed. Check the source before drawing any conclusion about harm.
The source did not state who this applies to in practice.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
This record has not been graded across any dimension yet. Treat the label above as provisional and read the source.
What is missing. This record has no bottom line, key findings, reported figures, evidence dimensions. That is a gap in the analysis, not a judgement about the study.
Targeting tumor cell plasticity is central to overcome drug resistance and metastasis. Through lineage-tracing and lineage-ablation studies, our team has previously shown hepatocellular carcinoma (HCC) cells marked by CD133 to represent a functional subset displaying dedifferentiated status with stemness traits, yet there are limited therapies effective for eradicating such resilient cell populations. Here, we explore the therapeutic potential of repurposing an existing drug estramustine phosphate (EMP) for targeting HCC plasticity through inhibiting MAP2, a gene uniquely enriched in CD133+ ‘HCC’ stemness subset but not in CD133+ ‘normal’ regenerative cells. MAP2 is transcriptionally activated by histone 3 lysine 27 acetylation and its upregulation correlates with aggressive clinical features. Mechanistically, MAP2 sustains tumor plasticity and transition to a mesenchymal state through inducing filamentous actin polymerization and YAP activation, which subsequently disrupts integrin expression and cell adhesions. Our research offers a promising opportunity for drug repurposing using EMP in combination with sorafenib to target HCC at its stemness roots. Cancer cell plasticity contributes to drug resistance and metastasis in liver cancer. Here, authors show that targeting MAP2 with estramustine phosphate disrupts cancer stemness and enhances sensitivity to sorafenib in hepatocellular carcinoma.