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BPQDs@Lipo-YSA Nanoplatform Triggers Mitophagy via PRKN/AKT1 to Drive Immunogenic Cell Death in Lung Adenocarcinoma.

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Title: BPQDs@Lipo-YSA Nanoplatform Triggers Mitophagy via PRKN/AKT1 to Drive Immunogenic Cell Death in Lung Adenocarcinoma.
Authors: Ai, Li1 (AUTHOR), Liu, Zhijuan1 (AUTHOR), Li, Ran1 (AUTHOR), Hu, Ying2 (AUTHOR) hy2002@126.com, Li, Yongxia1 (AUTHOR) liyongxia@kmmu.edu.cn
Source: Journal of Nanobiotechnology. 6/16/2025, Vol. 23 Issue 1, p1-19. 19p.
Subjects: Non-small-cell lung carcinoma, Electron microscope techniques, Medical sciences, Transmission electron microscopy, Light scattering
Abstract: Background: Lung adenocarcinoma, the most common type of non-small cell lung cancer (NSCLC), is a leading cause of cancer-related deaths globally due to its high incidence and treatment difficulty. Despite recent advancements in treatment methods, the prognosis for patients with advanced disease remains poor. Studies have shown that targeting mitophagy, the selective clearance of damaged mitochondria, can influence the sensitivity of cancer cells to treatment. Methods: In this study, we designed and synthesized BPQDs@Lipo-YSA, a novel nanomaterial, aimed at specifically inducing mitophagy in lung adenocarcinoma cells. The nanomaterial was characterized using techniques such as transmission electron microscopy (TEM) and dynamic light scattering (DLS). The ability of BPQDs@Lipo-YSA to induce mitophagy was evaluated using Western blot, immunofluorescence, and flow cytometry. Additionally, in vitro and in vivo experiments were conducted to investigate the impact of BPQDs@Lipo-YSA on lung adenocarcinoma cells through the induction of immunogenic cell death (ICD). Results: Experimental results showed that BPQDs@Lipo-YSA effectively induced mitophagy in lung adenocarcinoma cells by activating the PRKN/AKT1 pathway. More importantly, this induction of mitophagy significantly enhanced the cytotoxic effect on lung adenocarcinoma cells. In animal models, BPQDs@Lipo-YSA, by inducing ICD, markedly inhibited tumor growth and extended survival. Conclusions: This study reveals the potential value of BPQDs@Lipo-YSA in lung adenocarcinoma treatment through the induction of mitophagy and ICD. This finding provides theoretical and technical support for the development of new therapeutic strategies for lung adenocarcinoma. [ABSTRACT FROM AUTHOR]
Copyright of Journal of Nanobiotechnology is the property of BioMed Central and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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  Data: BPQDs@Lipo-YSA Nanoplatform Triggers Mitophagy via PRKN/AKT1 to Drive Immunogenic Cell Death in Lung Adenocarcinoma.
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  Data: <searchLink fieldCode="JN" term="%22Journal+of+Nanobiotechnology%22">Journal of Nanobiotechnology</searchLink>. 6/16/2025, Vol. 23 Issue 1, p1-19. 19p.
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  Data: <searchLink fieldCode="DE" term="%22Non-small-cell+lung+carcinoma%22">Non-small-cell lung carcinoma</searchLink><br /><searchLink fieldCode="DE" term="%22Electron+microscope+techniques%22">Electron microscope techniques</searchLink><br /><searchLink fieldCode="DE" term="%22Medical+sciences%22">Medical sciences</searchLink><br /><searchLink fieldCode="DE" term="%22Transmission+electron+microscopy%22">Transmission electron microscopy</searchLink><br /><searchLink fieldCode="DE" term="%22Light+scattering%22">Light scattering</searchLink>
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  Label: Abstract
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  Data: Background: Lung adenocarcinoma, the most common type of non-small cell lung cancer (NSCLC), is a leading cause of cancer-related deaths globally due to its high incidence and treatment difficulty. Despite recent advancements in treatment methods, the prognosis for patients with advanced disease remains poor. Studies have shown that targeting mitophagy, the selective clearance of damaged mitochondria, can influence the sensitivity of cancer cells to treatment. Methods: In this study, we designed and synthesized BPQDs@Lipo-YSA, a novel nanomaterial, aimed at specifically inducing mitophagy in lung adenocarcinoma cells. The nanomaterial was characterized using techniques such as transmission electron microscopy (TEM) and dynamic light scattering (DLS). The ability of BPQDs@Lipo-YSA to induce mitophagy was evaluated using Western blot, immunofluorescence, and flow cytometry. Additionally, in vitro and in vivo experiments were conducted to investigate the impact of BPQDs@Lipo-YSA on lung adenocarcinoma cells through the induction of immunogenic cell death (ICD). Results: Experimental results showed that BPQDs@Lipo-YSA effectively induced mitophagy in lung adenocarcinoma cells by activating the PRKN/AKT1 pathway. More importantly, this induction of mitophagy significantly enhanced the cytotoxic effect on lung adenocarcinoma cells. In animal models, BPQDs@Lipo-YSA, by inducing ICD, markedly inhibited tumor growth and extended survival. Conclusions: This study reveals the potential value of BPQDs@Lipo-YSA in lung adenocarcinoma treatment through the induction of mitophagy and ICD. This finding provides theoretical and technical support for the development of new therapeutic strategies for lung adenocarcinoma. [ABSTRACT FROM AUTHOR]
– Name: AbstractSuppliedCopyright
  Label:
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  Data: <i>Copyright of Journal of Nanobiotechnology is the property of BioMed Central and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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      – SubjectFull: Electron microscope techniques
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              Text: 6/16/2025
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