Interplay between programmed death-ligand 1 and non-coding RNAs

Soudeh Ghafouri-Fard1, Hamed Shoorei2,3, Bashdar Mahmud Hussen4,5

  • 1Department of Medical Genetics, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.

Frontiers in Immunology
|November 21, 2022
PubMed

Insights

Programmed death-ligand 1 (PD-L1) is key in immune suppression by cancer. Understanding its regulation by non-coding RNAs like miRNAs, lncRNAs, and circRNAs can improve cancer therapies and patient treatment selection.

Area of Science:

  • Immunology
  • Molecular Biology
  • Oncology

Background:

  • Programmed death-ligand 1 (PD-L1) is a transmembrane protein crucial for suppressing adaptive immune responses.
  • Cancer cells exploit PD-L1 to evade immune system attacks, making it a target for cancer therapies.
  • Modulating the PD1/PD-L1 axis is essential for releasing anti-tumor immune responses.

Purpose of the Study:

  • To review the interactions between non-coding RNAs (miRNAs, lncRNAs, circRNAs) and PD-L1 in cancer.
  • To summarize how these interactions influence the PD1/PD-L1 axis activity.
  • To overview the impact of these interactions on patient response to anti-cancer drugs.

Main Methods:

  • Literature review of recent studies on non-coding RNAs and PD-L1.
  • Analysis of interactions between specific transcripts (miRNAs, lncRNAs, circRNAs) and PD-L1.
  • Synthesis of findings regarding the role of these interactions in cancer immunity and drug response.

Main Results:

  • Non-coding RNAs, including miRNAs, lncRNAs, and circRNAs, have confirmed interactions with PD-L1.
  • These interactions play a significant role in modulating PD-L1 expression and function.
  • The interplay between non-coding RNAs and PD-L1 impacts the efficacy of cancer immunotherapies.

Conclusions:

  • Understanding non-coding RNA regulation of PD-L1 is vital for developing novel cancer treatments.
  • Identifying these interactions can aid in predicting patient responses to PD1/PD-L1 blockade therapies.
  • Further research into these mechanisms promises to enhance therapeutic strategies and patient outcomes in oncology.

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