Esophageal carcinoma cell-excreted exosomal uc.189 promotes lymphatic metastasis

Aging (Albany NY). 2021 May 23;13(10):13846-13858. doi: 10.18632/aging.202979. Epub 2021 May 23.

Abstract

Most cancers are old age-related diseases. Patients with lymphatic metastasis have an extremely poor prognosis in esophageal cancers (ECs). Previous studies showed ultraconserved RNAs are involved in tumorigenesis and ultraconserved RNA 189 (uc.189) served as an oncogene in cervical cancer, but the effect of exosomal uc.189 in esophageal squamous cell carcinoma (ESCC) remains undefined. This study revealed that uc.189 is closely correlated with lymph node (LN) metastasis and the number of lymphatic vessels in ESCC. ESCC-secreted exosomal uc.189 is transferred into human lymphatic endothelial cells (HLECs) to promote its proliferation, migration and tube formation to facilitate lymph node metastasis. Mechanistically, uc.189 regulated EPHA2 expression by directly binding to its 3'UTR region through dual-luciferase reporter assay. Over-expression and knockdown of EPHA2 could respectively rescue and simulate the effects induced by exosomal uc.189. Especially, the uc.189-EPHA2 axis activates the P38MAPK/VEGF-C pathway in HLECs. Finally, ESCC-secreted exosomal of uc.189 promotes HLECs sprouting in vitro, migration, and lymphangiogenesis. Thus, these findings suggested that exosomal uc.189 targets the EPHA2 of HLECs to promote lymphangiogenesis, and may represent a novel marker of diagnosis and treatment for ESCC patients in early stages.

Keywords: HLECs; exosomal uc.189; lymphangiogenesis; metastasis esophageal carcinoma.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Base Sequence
  • Cell Line, Tumor
  • Cell Movement / genetics
  • Cell Proliferation / genetics
  • Endothelial Cells / metabolism
  • Esophageal Neoplasms / genetics*
  • Esophageal Neoplasms / pathology*
  • Esophageal Squamous Cell Carcinoma / genetics
  • Esophageal Squamous Cell Carcinoma / pathology
  • Exosomes / genetics*
  • Exosomes / ultrastructure
  • Gene Expression Regulation, Neoplastic
  • Humans
  • Lymphangiogenesis / genetics
  • Lymphatic Metastasis / genetics*
  • Lymphatic Vessels / pathology
  • Models, Biological
  • RNA, Neoplasm / genetics*
  • RNA, Neoplasm / metabolism
  • Receptor, EphA2 / metabolism
  • Signal Transduction / genetics
  • Vascular Endothelial Growth Factor C / metabolism
  • p38 Mitogen-Activated Protein Kinases / metabolism

Substances

  • EPHA2 protein, human
  • RNA, Neoplasm
  • Vascular Endothelial Growth Factor C
  • Receptor, EphA2
  • p38 Mitogen-Activated Protein Kinases