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SCARA3 inhibits cell proliferation and EMT through AKT signaling pathway in lung cancer

Jeeho Kim1,2, Ho Jin You3,4, Chakyung Youn5

  • 1Laboratory of Genomic Instability and Cancer therapeutics and Department of Pharmacology, Chosun University School of Medicine, 375 Seosuk-Dong, Gwangju, 501-759, South Korea.

BMC Cancer
|May 16, 2022
PubMed
Abstract

Insights

Scavenger receptor class A member 3 (SCARA3) is decreased in lung cancer. Overexpressing SCARA3 inhibits tumor growth and enhances cisplatin treatment efficacy through AKT and JNK pathways, suggesting SCARA3 as a potential biomarker.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Scavenger receptor class A member 3 (SCARA3) expression is reduced in prostate cancer and myeloma.
  • The specific role of SCARA3 in various cancer types, including lung cancer, remains largely uncharacterized.

Purpose of the Study:

  • To investigate the functional role of SCARA3 in lung cancer.
  • To evaluate SCARA3 as a potential biomarker and therapeutic target in lung cancer.

Main Methods:

  • Analysis of SCARA3 expression in lung cancer datasets (TCGA), tissue microarrays, and cell lines.
  • Assessment of SCARA3's impact on lung cancer cell proliferation, migration, and invasion in vitro and in vivo (mouse xenograft model).
  • Evaluation of SCARA3's influence on epithelial-mesenchymal transition (EMT) markers and its interaction with cisplatin treatment via AKT and JNK pathways.

Main Results:

  • SCARA3 expression was found to be significantly downregulated in lung cancer tissues and cells.
  • Overexpression of SCARA3 suppressed lung cancer cell proliferation, migration, and invasion, and reduced EMT markers (β-catenin, vimentin, MMP9).
  • SCARA3 overexpression potentiated the anti-cancer effect of cisplatin, mediated through the AKT and JNK signaling pathways.

Conclusions:

  • SCARA3 is abnormally decreased in lung cancer, acting as a tumor suppressor.
  • SCARA3 overexpression inhibits tumor progression and sensitizes lung cancer cells to cisplatin, indicating its potential as a therapeutic target.
  • SCARA3 serves as a significant biomarker for lung cancer, and its induction may lead to effective treatment strategies.
Keywords:
AKT signalingLung CancerSCARA3Tumor growth

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