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The Downregulation of LSAMP Expression Promotes Lung Cancer Progression and Is Associated with Poor Survival

Chao-Yuan Chang1,2, Kuan-Li Wu1,3,4, Yung-Yun Chang3,5

  • 1Graduate Institute of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung 807, Taiwan.

Journal of Personalized Medicine
|July 2, 2021
PubMed

Insights

Limbic System Associated Membrane Protein (LSAMP) loss is linked to lung adenocarcinoma progression and poorer survival. LSAMP acts as a tumor suppressor, potentially offering new therapeutic strategies for lung cancer.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Lung cancer remains a leading cause of cancer-related mortality.
  • Effective therapeutic strategies for non-driver mutation lung cancer are limited.
  • Novel therapeutic targets are urgently needed for lung adenocarcinoma (LUAD).

Purpose of the Study:

  • To investigate the prognostic and therapeutic significance of IgLON family proteins in LUAD.
  • To identify potential molecular mechanisms underlying LSAMP downregulation in LUAD.
  • To explore the functional role of LSAMP in LUAD cell biology.

Main Methods:

  • Comparative analysis of LSAMP, NTM, and OPCML expression in LUAD tissues and public datasets (Oncomine®, TCGA).
  • Correlation analysis between LSAMP expression and patient overall survival.
  • Investigation of epigenetic regulations (methylation, miRNA, copy number variation) associated with LSAMP downregulation.
  • Functional studies involving LSAMP knockdown in LUAD cell lines to assess effects on migration, proliferation, and stemness.
  • Pathway network analysis to identify interacting molecules, such as NEGR1.

Main Results:

  • Loss of Limbic System Associated Membrane Protein (LSAMP) showed the strongest prognostic and therapeutic significance in LUAD progression compared to NTM and OPCML.
  • Lower expression of LSAMP and NTM, but not OPCML, was observed in LUAD tumors versus normal tissues.
  • Reduced LSAMP expression correlated with shorter overall survival in LUAD patients.
  • LSAMP downregulation was associated with hypermethylation and miR-143-3p upregulation.
  • LSAMP knockdown promoted LUAD cell migration via epithelial-mesenchymal transition (EMT), without affecting proliferation or stemness.

Conclusions:

  • LSAMP functions as a potential tumor suppressor in lung cancer.
  • LSAMP's role in regulating cancer cell migration via EMT presents a novel therapeutic target.
  • Further research into LSAMP's role in lung cancer tumorigenesis could lead to new treatment strategies.
Keywords:
EMTLSAMPlung adenocarcinoma

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