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Angelicin inhibits human lung carcinoma A549 cell growth and migration through regulating JNK and ERK pathways

Guangcai Li1, Yuan He2, Jun Yao2

  • 1Department of Respiratory Diseases, Tongji Hospital, Key Laboratory of Pulmonary Diseases of Health Ministry, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430000, P.R. China.

Oncology Reports
|October 18, 2016
PubMed

Insights

Angelicin inhibits human lung carcinoma growth and metastasis by inducing apoptosis and cell cycle arrest. It targets extracellular signal-regulated kinase (ERK) and c-Jun NH2-terminal kinase (JNK) signaling pathways, showing potential for non-small cell lung cancer (NSCLC) therapy.

Area of Science:

  • Pharmacology
  • Molecular Biology
  • Oncology

Background:

  • Angelicin is a photosensitizer with known anticancer properties.
  • The precise mechanisms of angelicin's action on human lung cancer remain largely unelucidated.

Purpose of the Study:

  • To investigate the effects and underlying mechanisms of angelicin on human lung carcinoma cell growth and metastasis.
  • To evaluate angelicin's therapeutic potential for non-small cell lung cancer (NSCLC).

Main Methods:

  • In vitro studies involving cell apoptosis, cell cycle arrest, and migration assays (Transwell).
  • Analysis of apoptosis-related proteins (Bax, Bcl-2, caspase-3, caspase-9) and cell cycle regulators (cyclins, Cdc2).
  • Assessment of matrix metalloproteinases (MMP2, MMP9) and E-cadherin expression.
  • Investigation of extracellular signal-regulated kinase (ERK) and c-Jun NH2-terminal kinase (JNK) signaling pathways.
  • In vivo xenograft and metastasis models using A549 cells.

Main Results:

  • Angelicin significantly inhibited NSCLC A549 cell proliferation, induced apoptosis, and caused cell cycle arrest in vitro.
  • Angelicin suppressed cell migration, downregulated Bcl-2, and upregulated Bax, cleaved caspase-3, and cleaved caspase-9.
  • Angelicin reduced cyclin B1, cyclin E1, Cdc2, MMP2, and MMP9 expression, while increasing E-cadherin.
  • Angelicin treatment led to increased phosphorylation of ERK1/2 and JNK1/2; inhibition of these pathways abrogated angelicin's effects.
  • In vivo models confirmed angelicin's significant inhibition of tumor growth and lung metastasis.

Conclusions:

  • Angelicin effectively inhibits human non-small cell lung cancer (NSCLC) cell growth and metastasis.
  • The mechanism involves the induction of apoptosis, cell cycle arrest, and modulation of key signaling pathways (ERK, JNK).
  • Angelicin demonstrates considerable potential as a therapeutic agent for NSCLC.

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