Inhaled rapamycin–doxorubicin nanoliposomes targeting senescent lung cancer cells in mice
An abstract reports that inhalable nanoliposomes carrying rapamycin and doxorubicin, aimed at senescent lung cancer cells, suppressed tumor growth in a chemoresistant mouse model without appreciable systemic toxicity. [1]
Automatic summary · not editorially reviewed
The key findings
The abstract describes an inhalable nanoliposome co-encapsulating rapamycin and doxorubicin, with an aptamer targeting L1 cell adhesion molecule. [1]
After inhalation, the nanoliposomes are reported to cross the mucus barrier and target senescent lung cancer cells via L1 cell adhesion molecule recognition. [1]
In a chemoresistant mouse model, inhaled nanoliposomes significantly suppressed tumor growth without appreciable systemic toxicity. [1]
The source at a glance
- Study type / format
- Preclinical abstract (mouse model)
- Population / context
- Senescent lung cancer cells in a chemoresistant mouse model
- Summary based on
- Study abstract
- Original publication
- September 23, 2026
Mucus barrier and therapy-induced senescence in lung cancer
The abstract states that lung cancer therapy is severely hindered by the pulmonary mucus barrier and by chemotherapy resistance driven by therapy-induced senescence after DNA-damaging agents. The proposed approach is an inhalable nanoliposome, DR@DPPC-Apt, built from dipalmitoyl phosphatidylcholine with a cholesterol-modified aptamer that targets L1 cell adhesion molecule, and co-encapsulating rapamycin and doxorubicin.
Supporting source [1]
Inhaled uptake and senescence reversal in the mouse model
According to the abstract, after noninvasive inhalation the nanoliposomes cross the mucus barrier and are taken up by senescent lung cancer cells through aptamer recognition of overexpressed L1 cell adhesion molecule, concentrating drugs at the tumor. Intratumorally, rapamycin is said to inhibit the mammalian target of rapamycin pathway, reversing the senescent phenotype, enhancing drug retention, hyperactivating autophagy and blocking senescence propagation, which resensitizes cells to chemotherapy. In a chemoresistant mouse model, inhalation significantly suppressed tumor growth without appreciable systemic toxicity.
Supporting source [1]
Abstract-only preclinical scope of the nanoliposome report
These results come from a chemoresistant lung cancer mouse model described in the abstract; the abstract does not report sample size, follow-up duration or detailed toxicity measures. The full text was not reviewed. The abstract calls the strategy promising for clinical translation, but no human data are presented, and the described effects are preclinical.
Supporting source [1]
How to interpret this
Abstract only; the full text was not reviewed. Results are from a mouse model, and sample size, follow-up and detailed toxicity data are not reported in the abstract. No human data are presented.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Man Y, Liu Y, Liu Y, Wu J, Tan Y, Cheng Z, Lee LP, Chen QW, Liu Z. · europepmc.org · September 23, 2026