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Peer-reviewedCC BY 4.0Advanced Science

Nanoparticle‐Mediated TIPE1 mRNA Delivery Enhances Paclitaxel Sensitivity in Triple‐Negative Breast Cancer by Modulating RAB7A Ubiquitination‐Associated Stability and Autophagy

  • Wei Hu1
  • Qishuai Chen1
  • Yan Ma2
  • Yang Liu3
  • Xianing Dong3
  • Wenjuan Wei2
  • Jianxin Du2
  • Shusheng Qiu1
  • Maojin Tian4,5
  • Peiqing Zhao2
5 affiliations
  1. 1Department of Breast Surgery Zibo Central Hospital Affiliated to Binzhou Medical University Zibo China
  2. 2Center of Translational Medicine Zibo Central Hospital Affiliated to Binzhou Medical University Zibo China
  3. 3School of Medical Laboratory Shandong Second Medical University Zibo China
  4. 4Department of Critical Care Medicine Zibo Central Hospital Affiliated to Binzhou Medical University Zibo China
  5. 5Department of Microbiology Laboratory Zibo Municipal Hospital Zibo China
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Abstract

Acquired paclitaxel (PTX) resistance remains a major obstacle in triple‐negative breast cancer (TNBC) treatment. This study investigated TIPE1's role in regulating autophagy and PTX sensitivity and developed ROS‐responsive TIPE1 mRNA‐loaded nanoparticles (TIPE1m NPs) as a therapeutic strategy. PTX‐resistant TNBC cell lines were established, and integrated transcriptomic and proteomic analyses were performed. TIPE1 was downregulated in resistant cells, while higher TNFAIP8L1 expression in public breast cancer cohorts was associated with better survival and improved PTX response. Mechanistically, TIPE1 overexpression was associated with ubiquitination‐related reduction in the stability of the small GTPase RAB7A, leading to impaired autophagic flux, increased ROS accumulation, and enhanced PTX‐induced apoptosis. Conversely, TIPE1 knockdown stabilized RAB7A, enhanced autophagy, and increased PTX tolerance. ROS‐responsive TIPE1m NPs were constructed to restore TIPE1 expression in resistant cells. TIPE1m NPs suppressed autophagy, increased ROS, and enhanced PTX‐induced apoptosis in vitro. In PTX‐resistant xenografts, combined TIPE1m NPs and PTX treatment suppressed tumor growth without obvious systemic toxicity. These findings identify the TIPE1–RAB7A–autophagy axis as a potential therapeutic target and support TIPE1 mRNA delivery as a strategy to overcome PTX resistance in TNBC.

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Cite

BibTeXRIS
BibTeX
@article{hu2026nanoparticlemediated,
  title = {{Nanoparticle‐Mediated TIPE1 mRNA Delivery Enhances Paclitaxel Sensitivity in Triple‐Negative Breast Cancer by Modulating RAB7A Ubiquitination‐Associated Stability and Autophagy}},
  author = {Wei Hu and Qishuai Chen and Yan Ma and Yang Liu and Xianing Dong and Wenjuan Wei and Jianxin Du and Shusheng Qiu and Maojin Tian and Peiqing Zhao},
  journal = {Advanced Science},
  year = {2026},
  month = aug,
  doi = {10.1002/advs.76975},
  url = {https://doi.org/10.1002/advs.76975},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Nanoparticle‐Mediated TIPE1 mRNA Delivery Enhances Paclitaxel Sensitivity in Triple‐Negative Breast Cancer by Modulating RAB7A Ubiquitination‐Associated Stability and Autophagy
AU  - Wei Hu
AU  - Qishuai Chen
AU  - Yan Ma
AU  - Yang Liu
AU  - Xianing Dong
AU  - Wenjuan Wei
AU  - Jianxin Du
AU  - Shusheng Qiu
AU  - Maojin Tian
AU  - Peiqing Zhao
PY  - 2026
DA  - 2026/08/06
JO  - Advanced Science
DO  - 10.1002/advs.76975
UR  - https://doi.org/10.1002/advs.76975
AB  - Acquired paclitaxel (PTX) resistance remains a major obstacle in triple‐negative breast cancer (TNBC) treatment. This study investigated TIPE1's role in regulating autophagy and PTX sensitivity and developed ROS‐responsive TIPE1 mRNA‐loaded nanoparticles (TIPE1m NPs) as a therapeutic strategy. PTX‐resistant TNBC cell lines were established, and integrated transcriptomic and proteomic analyses were performed. TIPE1 was downregulated in resistant cells, while higher TNFAIP8L1 expression in public breast cancer cohorts was associated with better survival and improved PTX response. Mechanistically, TIPE1 overexpression was associated with ubiquitination‐related reduction in the stability of the small GTPase RAB7A, leading to impaired autophagic flux, increased ROS accumulation, and enhanced PTX‐induced apoptosis. Conversely, TIPE1 knockdown stabilized RAB7A, enhanced autophagy, and increased PTX tolerance. ROS‐responsive TIPE1m NPs were constructed to restore TIPE1 expression in resistant cells. TIPE1m NPs suppressed autophagy, increased ROS, and enhanced PTX‐induced apoptosis in vitro. In PTX‐resistant xenografts, combined TIPE1m NPs and PTX treatment suppressed tumor growth without obvious systemic toxicity. These findings identify the TIPE1–RAB7A–autophagy axis as a potential therapeutic target and support TIPE1 mRNA delivery as a strategy to overcome PTX resistance in TNBC.
SN  - 2198-3844
ER  -