CEACAM1 increased the lymphangiogenesis through miR-423-5p and NF- kB in Non-Small Cell Lung Cancer

  • 0Department of Thoracocardiac Surgery, 920th Hospital of Joint Logistics Support Force of Chinese People's Liberation Army, Kunming, Yunnan, China.

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Summary

This summary is machine-generated.

Carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1) promotes lymph node metastasis in non-small cell lung cancer (NSCLC) by activating the NF-κB pathway. MiR-423-5p represses CEACAM1, suggesting CEACAM1 as a potential therapeutic target in NSCLC.

Area Of Science

  • Oncology
  • Molecular Biology
  • Cancer Research

Background

  • Lung cancer, particularly non-small cell lung cancer (NSCLC), is a leading cause of cancer mortality.
  • Lymph node metastasis is a critical determinant of NSCLC staging and patient prognosis.
  • Carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1) is implicated in various cancers, but its role in NSCLC lymphangiogenesis is underexplored.

Purpose Of The Study

  • To investigate the influence of CEACAM1 on lymphangiogenesis in NSCLC.
  • To elucidate the molecular mechanisms by which CEACAM1 affects lymphangiogenesis.
  • To explore the potential of CEACAM1 as a therapeutic target for NSCLC.

Main Methods

  • Immunohistochemistry and quantitative PCR (qPCR) were used to assess CEACAM1, CD31, LVYE1, and hsa-miR-423-5p expression in patient samples.
  • Western blot analysis was performed to detect lymphangiogenesis-associated proteins and NF-κB pathway cytokines.
  • A tube formation assay was employed to evaluate lymphangiogenesis, and a dual luciferase assay confirmed the interaction between CEACAM1 and hsa-miR-423-5p.

Main Results

  • CEACAM1 expression was positively correlated with angiogenesis and lymphangiogenesis in NSCLC.
  • CEACAM1 was found to promote lymphangiogenesis, while hsa-miR-423-5p overexpression inhibited it by targeting CEACAM1.
  • CEACAM1 activation of the NF-κB pathway was identified as a key mechanism promoting lymphangiogenesis.

Conclusions

  • CEACAM1 enhances lymphangiogenesis in NSCLC through NF-κB pathway activation.
  • CEACAM1-mediated lymphangiogenesis is negatively regulated by miR-423-5p.
  • CEACAM1 represents a promising therapeutic marker for NSCLC treatment.

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