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Related Concept Videos

The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

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The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
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Overview of Cell Death01:30

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Cell death is an essential process where the body gets rid of old or damaged cells. Cell proliferation and death need to be balanced, as an imbalance between the two may lead to cancer or autoimmune diseases.
Cell death was observed in the early 19th century, but there was no experimental evidence to prove it. In 1842, Carl Vogt first discovered cell death in a metamorphic toad; however, it was not termed ‘cell death.’ Scientists discovered different cell death pathways only in the...
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The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

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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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Necrosis01:16

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Necrosis is considered as an “accidental” or unexpected form of cell death that ends in cell lysis. The first noticeable mention of “necrosis” was in 1859 when Rudolf Virchow used this term to describe advanced tissue breakdown in his compilation titled “Cell Pathology”.
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Apoptosis01:30

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Apoptosis is a combination of two Greek words, 'apo' and 'ptosis,' meaning separation and falling off, respectively. Hippocrates used this word to describe gangrene, which was caused due to bandaging of fractured bones. Apoptosis was distinguished from necrosis in 1970 when John Kerr reported observations of morphological changes occurring during apoptosis. During one experiment, he observed that the disruption of blood supply to the liver tissue resulted in a size...
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Autophagic Cell Death

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Christian de Duve discovered “autophagy,” a process in which cellular components are engulfed by membrane-bound organelles called autophagosomes. The autophagosomes then fuse with lysosomes to digest the enclosed contents. Autophagy is generally activated in cells to prevent cell death. However, cell death is triggered when the damage is beyond repair.
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Programmed death-ligand 1 nuclear translocation: A novel perspective from membrane localization to nuclear function.

Jin Tian1, Xiaoyue Zhang2, Xiaoyuan Sun3

  • 1Qingdao Hiser Hospital Affiliated of Qingdao University (Qingdao Traditional Chinese Medicine Hospital), Qingdao, Shandong, China.

International Journal of Cancer
|March 24, 2026
PubMed
Summary

Programmed death-ligand 1 (PD-L1) moves into the nucleus, impacting tumor growth via non-immune pathways. Understanding nuclear PD-L1 (nPD-L1) mechanisms is crucial for developing targeted cancer therapies.

Keywords:
HDAC2 inhibitorPD‐L1 nuclear translocationnon‐immune functionspost‐translational modifications (PTMs)therapy resistance

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Area of Science:

  • Immunology
  • Molecular Biology
  • Oncology

Background:

  • Membrane-bound programmed death-ligand 1 (PD-L1) is a known immune checkpoint molecule mediating tumor immune evasion.
  • Emerging research indicates PD-L1 translocates to the nucleus (nuclear PD-L1, nPD-L1), influencing tumor progression through non-immune mechanisms.

Purpose of the Study:

  • To systematically review the molecular mechanisms of PD-L1 nuclear translocation.
  • To summarize the biological functions and roles of nPD-L1 in the tumor microenvironment.
  • To explore the potential of nPD-L1 as a biomarker and therapeutic target.

Main Methods:

  • Review of recent studies on PD-L1 nuclear translocation.
  • Analysis of molecular pathways involved in nPD-L1 regulation (acetylation, endocytosis, nuclear transport, deacetylation, ubiquitination).
  • Examination of nPD-L1's role in gene regulation, angiogenesis, DNA repair, and other cellular processes.

Main Results:

  • PD-L1 nuclear translocation is regulated by p300, Huntingtin-interacting protein 1-related protein, Vimentin-importin α/β, and histone deacetylase 2.
  • nPD-L1 influences target genes like early growth response 1, affecting angiogenesis and immune evasion.
  • nPD-L1 has diverse non-immune functions, including DNA repair and pyroptosis, with both pro-tumorigenic and tumor-suppressive roles.

Conclusions:

  • Nuclear translocation of PD-L1 represents a novel mechanism in cancer progression and immune evasion.
  • Understanding nPD-L1's complex roles and regulatory pathways is vital for translational research and targeted therapy development.
  • MIB2-mediated ubiquitination and inhibitors like BMS1166 offer potential therapeutic strategies targeting PD-L1 localization.