ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
Pristimerin Promotes Ubiquitination of HSPA8 and Activates the VAV1/ERK Pathway to Suppress TNBC Proliferation.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The trial behind it
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Who cites it
8 citing papers in PubMed.
- Xanthatin Targets CISD1 to Drive Ferroptosis and Mitophagy as a Dual Anticancer Strategy in Triple-Negative Breast Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- SUMOylation is destined for regulatory T cell-related immune dysregulation.Cell death discovery · 2026Review
- Chondroitin sulfate alleviates osteoarthritis by upregulating HSPA8 to inhibit chondrocyte ferroptosis.PloS one · 2026Article
- Stage-Specific Regulation of Ubiquitination Modifications and Prospects for Targeted Therapy in Triple-Negative Breast Cancer.Oncology research · 2026Review
- Autophagy-Related Proteins in Triple-Negative Breast Cancer: From Molecular Insights to Therapeutic Applications.International journal of molecular sciences · 2025Review
- Pristimerin Promotes Ubiquitination of HSPA8 and Activates the VAV1/ERK Pathway to Suppress TNBC Proliferation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The ubiquitination-autophagy axis in cancer therapy resistance: mechanistic insights and therapeutic opportunities.Frontiers in pharmacology · 2025Review
- Article
Corrections and comments
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Authors and funding
12 authors.
Funding
Abstract
Triple-negative breast cancer (TNBC) is a subtype of breast cancer with a poor prognosis. The natural compound pristimerin has shown promising anti-tumor effect. Here, it is found that pristimerin significantly triggered the activation of autophagy initiation and induced apoptosis in TNBC. Mechanistically, RNA sequencing revealed that pristimerin activated mitogen-activated protein kinase/extracelluar regulated protein kinases (MAPK/ERK) pathway. Drug affinity responsive target stability and mass spectrometry techniques are employed to confirm the direct binding target of pristimerin. Heat shock protein family A member 8 (HSPA8) is identified and verified by cellular thermal shift assays and surface plasmon resonance assays. The further results suggested that pristimerin promoted the ubiquitination and degradation of HSPA8, leading to a decrease in the degradation of Vac Guanine Nucleotide Exchange Factor 1 (VAV1), a downstream client protein of HSPA8 which plays a crucial role in activating the ERK pathway. Importantly, knockdown of HSPA8 or VAV1 significantly impaired the anticancer activity of pristimerin on TNBC cells. Additionally, pristimerin significantly inhibited the migration and invasion of TNBC cells and enhanced the sensitivity of TNBC cells to doxorubicin. Collectively, this study provides the initial evidence that pristimerin directly targets HSPA8 to activate the VAV1/ERK pathway, thereby promoting cell autophagy and apoptosis.
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Registered trials
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