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Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
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Cells respond to damage and stress through highly coordinated processes that decide whether they survive or undergo controlled self-destruction. Two major pathways involved in this regulation are apoptosis, a type of programmed cell death, and autophagy, a survival mechanism that helps cells adapt to adverse conditions.ApoptosisApoptosis removes aged or injured cells to maintain tissue balance. During this process, the cell shrinks, chromatin condenses and fragments, and membrane-bound...
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Autophagy01:27

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Autophagy is a self-digesting process by which a cell protects itself from threats both within and outside the cell, ranging from abnormal proteins to invading bacteria. In this process, obsolete components of the cell and invading microbes are degraded by hydrolytic enzymes active in an acidic environment of the lysosomal lumen.
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Delivery Pathways to the Lysosome01:36

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Eukaryotic cells use different mechanisms to eliminate toxic waste obsolete and worn-out substances. Lysosomes play a pivotal role in this, and hence, these substances are carried to the lysosome from other parts of the cell and extracellular space through different pathways. The most elaborately studied pathways to the lysosome are the endocytic pathways.
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Cells undergoing apoptosis form apoptotic bodies that must be removed immediately to prevent inflammation, autoimmune diseases, and necrosis. Phagocytosis is carried out by professional phagocytes such as macrophages or  immature dendritic cells. Non-professional phagocytes such as  epithelial cells and fibroblasts also take part in this process; however, they are not as effective as professional phagocytes. 
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An Integrated System to Remotely Trigger Intracellular Signal Transduction by Upconversion Nanoparticle-mediated Kinase Photoactivation
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Near-Infrared Upconversion Modulation of Intracellular Protons for Autophagy-Induced Apoptosis.

Tao Jia1, Xinyu Wang1, Jun Zeng1

  • 1MIIT Key Laboratory of Critical Materials Technology for New Energy Conversion and Storage, School of Chemistry and Chemical Engineering, Harbin Institute of Technology, Harbin, People's Republic of China.

Advanced Materials (Deerfield Beach, Fla.)
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PubMed
Summary
This summary is machine-generated.

This study presents a novel nanoscale system for controlled proton delivery to tumors using near-infrared light. This approach effectively reduces tumor growth and triggers cancer cell death via proton-mediated autophagy-induced apoptosis (PAA).

Keywords:
autophagy‐induced apoptosisphotoacidprotontumor acidification visual quantificationupconversion

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Area of Science:

  • Biomedical Engineering
  • Nanotechnology
  • Cancer Therapeutics

Background:

  • Intracellular pH is crucial for cancer cell function, making pH modulation a potential therapeutic strategy.
  • Precise spatiotemporal control of proton levels in tumors remains a significant challenge in cancer therapy.

Purpose of the Study:

  • To develop a near-infrared (NIR)-controlled nanoscale proton delivery system for precise cancer treatment.
  • To investigate the efficacy of proton delivery in suppressing tumor growth and inducing cancer cell apoptosis.

Main Methods:

  • Utilized upconversion nanoparticles (UCNPs) coated with photoacid (PA) and ferrocene (Fc) for proton delivery.
  • Activated proton release in vivo using 980 nm NIR stimulation, leading to tumor microenvironment acidification.
  • Incorporated Fc for real-time visual quantification of proton accumulation via luminescence changes.

Main Results:

  • NIR stimulation triggered transient H+ release, reducing tumor cell glucose uptake by 50% and suppressing mTOR signaling.
  • Induced excessive autophagy leading to mitochondrial dysfunction and apoptosis, termed proton-mediated autophagy-induced apoptosis (PAA).
  • Achieved a six-fold reduction in tumor weight and elevated proton levels in glioma following intravenous administration.

Conclusions:

  • Established a spatiotemporally controlled platform for intratumoral proton dynamics using NIR-activated UCNPs.
  • Demonstrated the potential of precision cancer theranostics through non-invasive NIR irradiation.
  • The developed nanoagent effectively triggers PAA, offering a promising strategy for glioma treatment.