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Related Concept Videos

Activation of Integrins01:15

Activation of Integrins

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Integrins bind ligands and transmit information from outside the cell to inside or vice-versa through an "outside-in signaling" or "inside-out signaling."
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Integrins01:10

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Animal and protozoan cells do not have cell walls to help maintain shape and provide structural stability. Instead, these eukaryotic cells secrete a sticky mass of carbohydrates and proteins into the spaces between adjacent cells. This network of proteins and molecules is called an extracellular matrix or ECM.
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Antiepileptic drugs, such as levetiracetam (Keppra) and brivaracetam (Briviact), have emerged as crucial tools in managing epilepsy. These medications exert their therapeutic effects by targeting the synaptic vesicle protein SV2A, a transmembrane glycoprotein primarily found in the brain.
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The Tumor Microenvironment02:17

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Every normal cell or tissue is embedded in a complex local environment called stroma, consisting of different cell types, a basal membrane, and blood vessels. As normal cells mutate and develop into cancer cells, their local environment also changes to allow cancer progression. The tumor microenvironment (TME) consists of a complex cellular matrix of stromal cells and the developing tumor. The cross-talk between cancer cells and surrounding stromal cells is critical to disrupt normal tissue...
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Nonsense-mediated mRNA Decay02:27

Nonsense-mediated mRNA Decay

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The Upf proteins that carry out nonsense-mediated decay (NMD) are found in all eukaryotic organisms, including humans. Each protein has an individual role, but they need to work in collaboration. Upf1 is an ATP-dependent RNA helicase that unwinds the RNA helix. Because Upf1 can unwind any RNA, Upf2 and Upf3 are required to help Upf1 discriminate between nonsense and normal mRNAs.
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Tension Gauge Tether Probes for Quantifying Growth Factor Mediated Integrin Mechanics and Adhesion
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Integrin-Mediated TGFβ Activation Modulates the Tumour Microenvironment.

Nicholas F Brown1, John F Marshall2

  • 1Centre for Tumour Biology, Barts Cancer Institute, Cancer Research UK Centre of Excellence, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, UK.

Cancers
|August 24, 2019
PubMed
Summary

Transforming growth factor-beta (TGFβ) has dual roles in cancer, acting as a suppressor early on and a promoter later. Targeting integrins may enhance cancer immunotherapies by modulating TGFβ activation.

Keywords:
TGFβintegrinstumour microenvironmentαvβ6

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Area of Science:

  • Oncology
  • Immunology
  • Cell Biology

Background:

  • Transforming growth factor-beta (TGFβ) exhibits context-dependent roles in cancer, acting as a tumor suppressor in early stages and a promoter in established tumors.
  • TGFβ signaling is crucial in the tumor microenvironment (TME), influencing processes like epithelial-to-mesenchymal transition (EMT), cancer-associated fibroblast (CAF) formation, and angiogenesis.
  • Latent TGFβ requires local activation within the TME to exert its functions, with αv-integrins identified as key activators.

Purpose of the Study:

  • To review the multifaceted role of TGFβ in cancer progression and immune evasion.
  • To elucidate the function of integrins in activating TGFβ within the TME.
  • To explore the therapeutic potential of targeting integrins to enhance anti-cancer immunotherapies.

Main Methods:

  • Literature review of studies on TGFβ, integrins, and the tumor microenvironment.
  • Analysis of mechanisms by which TGFβ influences cancer and immune surveillance.
  • Examination of the role of integrin-mediated TGFβ activation in immune suppression.

Main Results:

  • TGFβ suppresses normal tissue and early tumors but promotes established cancers via mechanisms including EMT and angiogenesis.
  • TGFβ is a potent inhibitor of T-cell-mediated immune surveillance and contributes to immunotherapy resistance.
  • Integrins, particularly αv-integrins, are critical for activating latent TGFβ in the TME.

Conclusions:

  • TGFβ's dual role necessitates understanding its activation mechanisms in the TME.
  • Integrin-mediated TGFβ activation contributes to an immunosuppressive TME.
  • Targeting integrins represents a promising strategy to overcome TGFβ-induced immune suppression and augment cancer immunotherapy efficacy.