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m6A-methylated KCTD21-AS1 regulates macrophage phagocytosis through CD47 and cell autophagy through TIPR

Dong-Min Liang1,2, You-Jie Li1, Jia-Xiang Zhang1

  • 1Department of Biochemistry and Molecular Biology, Binzhou Medical University, YanTai, Shandong, 264003, PR China.

Communications Biology
|February 21, 2024
PubMed

Insights

Long noncoding RNA KCTD21-AS1 promotes non-small cell lung cancer (NSCLC) proliferation by regulating CD47 and TIPRL. MicroRNA miR-519d-5p inhibits NSCLC via these targets, offering a potential therapeutic strategy.

Area of Science:

  • Immunology
  • Molecular Biology
  • Oncology

Background:

  • Immune checkpoint CD47/SIRPα blockade enhances macrophage phagocytosis for cancer immunotherapy.
  • The role of CD47-related noncoding RNAs in regulating macrophage phagocytosis and lung cancer progression is not fully understood.

Purpose of the Study:

  • To investigate the impact of long noncoding RNA (lncRNA) KCTD21-AS1 on macrophage phagocytosis via CD47 and non-small cell lung cancer (NSCLC) proliferation via TIPRL.
  • To explore the regulatory network involving KCTD21-AS1, miR-519d-5p, CD47, and TIPRL in NSCLC.

Main Methods:

  • Analysis of lncRNA KCTD21-AS1 expression in NSCLC tissues.
  • Investigation of the interaction between KCTD21-AS1, miR-519d-5p, CD47, and TIPRL using molecular biology techniques.
  • Assessment of macrophage phagocytosis and cancer cell proliferation and autophagy.

Main Results:

  • KCTD21-AS1 expression is elevated in NSCLC and linked to poor patient survival.
  • KCTD21-AS1 and its m6A modification promote NSCLC cell proliferation.
  • miR-519d-5p suppresses NSCLC proliferation and metastasis by regulating CD47 and TIPRL.
  • KCTD21-AS1 acts as a competing endogenous RNA (ceRNA) for miR-519d-5p, modulating CD47 and TIPRL expression, subsequently affecting macrophage phagocytosis and cancer cell autophagy.
  • Low miR-519d-5p and high TIPRL or CD47 levels correlate with poor NSCLC patient survival.

Conclusions:

  • KCTD21-AS1 and its m6A modification promote NSCLC proliferation, while miR-519d-5p inhibits it by regulating CD47 and TIPRL.
  • This regulatory axis influences macrophage phagocytosis and cancer cell autophagy.
  • Targeting KCTD21-AS1 or enhancing miR-519d-5p presents a potential therapeutic strategy for NSCLC by modulating CD47 and TIPRL.

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