Cancer, Stress, Anesthesia, and Immune Response / Nanoplatforms for Cancer Theranostics / Cancer Research and Treatments · Journal article
Journal of Nanobiotechnology · August 13, 2026
Early or partial results. Treat as a signal, not a conclusion.
This is a preclinical proof-of-concept study demonstrating that a novel acid-responsive nanoparticle (La₂O₃@PDA/PTX) combining lanthanum oxide, polydopamine, and paclitaxel inhibits lung tumor growth in subcutaneous and metastatic mouse models via ROS generation, cell-cycle arrest, and TNF/NF-κB pathway modulation. The work is mechanistically detailed but remains early-stage; translation to human efficacy and safety is not yet established.
Preclinical in vivo study. Lung cancer models with subcutaneous and metastatic tumors; animal studies.. Intervention: La₂O₃@PDA/PTX nanoparticle (lanthanum oxide, polydopamine, and paclitaxel).
La₂O₃@PDA/PTX nanoparticle demonstrated excellent aqueous stability, high biocompatibility, and low toxicity in vitro. Nanoparticle increased intracellular ROS, induced G2/M cell-cycle arrest, and regulated apoptosis-related proteins Ki67, Bcl-2, and Bax. Treatment increased NF-κB p65 phosphorylation and modulated TNF/NF-κB associated signaling with changes in tumor-associated cytokines and T-cell immunofluorescence.
La₂O₃@PDA/PTX nanoparticle demonstrated excellent aqueous stability, high biocompatibility, and low toxicity in vitro. Effectively inhibited progression of both subcutaneous and metastatic tumors with no significant adverse effects on major organs or peripheral blood parameters.
This preclinical result supports further development of the nanoparticle approach but cannot yet guide clinical practice. Transition to phase 1 human studies would be the next step to assess feasibility, safety, and initial efficacy signals.
Preclinical in vivo study of a novel nanoparticle in tumor models with mechanistic endpoints and biomarkers, but no human data, clinical outcomes, or comparison to standard therapy.
As stated by the source record.
This preclinical result supports further development of the nanoparticle approach but cannot yet guide clinical practice. Transition to phase 1 human studies would be the next step to assess feasibility, safety, and initial efficacy signals.
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.
What is missing. This record has no reported figures. That is a gap in the analysis, not a judgement about the study.
Lung cancer is one of the most common malignant tumors, but traditional treatments, particularly chemotherapy, often face significant challenges, including drug resistance and high systemic toxicity. In this study, we developed a novel acid responsive nanoparticle, La₂O₃@PDA/PTX, by combining lanthanum oxide (La₂O₃), polydopamine (PDA), and paclitaxel (PTX). This nanoparticle demonstrated excellent aqueous stability, high biocompatibility, and low toxicity. Benefiting from its structural design, the nanoparticle enables targeted delivery of PTX while simultaneously elevating intracellular reactive oxygen species (ROS) levels, which synergistically exacerbates oxidative stress injury within tumor cells. Mechanistically, La₂O₃@PDA/PTX inhibited tumor growth and induced apoptosis by increasing intracellular ROS, inducing G2/M cell-cycle arrest, and regulating proliferation and apoptosis related proteins, including Ki67, Bcl-2, and Bax. At the signaling level, La₂O₃@PDA/PTX increased NF-κB p65 phosphorylation and modulated TNF/NF-κB associated signaling, accompanied by changes in tumor associated cytokines and T-cell associated immunofluorescence signals. Furthermore, it effectively inhibited the progression of both subcutaneous and metastatic tumors with no significant adverse effects on major organs or peripheral blood parameters, showing great promise for future translational research. Collectively, this work presents an acid responsive therapeutic strategy combining ROS enhancement, chemotherapy, and TNF/NF-κB associated signaling modulation for lung cancer treatment.
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