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Oridonin represses lung cancer cell proliferation and migration by modulating AFAP1-AS1/IGF2BP1

Min Chen1, Yahui Shen2

  • 1Department of Respiratory and Critical Care Medicine, Taizhou People's Hospital Affiliated to Nanjing Medical University, Taizhou, Jiangsu 225300, China. yzcmhx@163.com.

Cellular and Molecular Biology (Noisy-Le-Grand, France)
|June 5, 2024
PubMed

Insights

Oridonin, a natural compound, inhibits lung cancer progression by downregulating AFAP1-AS1 and IGF2BP1. This discovery highlights a new therapeutic pathway for lung cancer treatment.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Oridonin, a compound from Rabdosia rubescens, exhibits anticancer properties.
  • Long non-coding RNA AFAP1-AS1 promotes lung cancer, but its interaction with oridonin is unknown.

Purpose of the Study:

  • To investigate oridonin's efficacy in lung cancer.
  • To elucidate oridonin's mechanism of action involving AFAP1-AS1 in lung cancer cells.

Main Methods:

  • Cell proliferation, migration, and invasion assays (MTT, wound healing, Transwell).
  • Analysis of AFAP1-AS1 and IGF2BP1 expression.
  • RNA immunoprecipitation (RIP) assay and in vivo tumor growth studies.

Main Results:

  • Oridonin suppressed lung cancer cell proliferation, migration, and invasion.
  • Oridonin downregulated AFAP1-AS1 expression; AFAP1-AS1 overexpression reversed oridonin's effects.
  • AFAP1-AS1 interacts with IGF2BP1; oridonin reduced IGF2BP1 levels, which was reversed by AFAP1-AS1 overexpression.
  • Overexpressed IGF2BP1 counteracted oridonin's inhibitory effects.
  • In vivo studies confirmed oridonin's tumor growth inhibition.

Conclusions:

  • Oridonin inhibits lung cancer cell proliferation and migration by modulating the AFAP1-AS1/IGF2BP1 pathway.
  • The AFAP1-AS1/IGF2BP1 axis represents a potential therapeutic target for lung cancer, particularly in conjunction with oridonin treatment.

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