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Induction and Analysis of Epithelial to Mesenchymal Transition
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ELTD1 Promotes Gastric Cancer Cell Proliferation, Invasion and Epithelial-Mesenchymal Transition Through MAPK/ERK

Bo Sun1, Fang-Jing Zhong1

  • 1Department of Surgery, Xiangya Hospital, Central South University, Changsha, Hunan, People's Republic of China.

International Journal of General Medicine
|September 3, 2021
PubMed
Abstract

Insights

Epidermal growth factor, latrophilin and seven-transmembrane domain-containing 1 (ELTD1) promotes gastric cancer (GC) metastasis by activating MAPK/ERK signaling and inhibiting CSK. High ELTD1 expression predicts poor prognosis in GC patients.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Gastric cancer (GC) metastasis remains a primary cause of patient mortality.
  • The molecular mechanisms driving GC metastasis are complex and not fully understood.
  • Epidermal growth factor, latrophilin and seven-transmembrane domain-containing 1 (ELTD1) has been implicated in cancer metastasis, but its role in GC is unexplored.

Purpose of the Study:

  • To investigate the expression and function of ELTD1 in gastric cancer.
  • To elucidate the molecular mechanism by which ELTD1 influences GC progression.
  • To evaluate ELTD1 as a prognostic biomarker for GC patients.

Main Methods:

  • ELTD1 expression analysis in GC tissues and public databases (TCGA, Oncomine, GEO).
  • In vitro and in vivo experiments to assess the effects of ELTD1 on GC cell proliferation, migration, invasion, and metastasis.
  • Investigation of ELTD1's mechanism of action, including its interaction with C-terminal Src kinase (CSK) and its effect on MAPK/ERK signaling.
  • Correlation analysis between ELTD1 expression and overall survival in GC patients.

Main Results:

  • ELTD1 is significantly upregulated in GC tissues.
  • ELTD1 knockdown inhibits GC cell proliferation, migration, invasion, tumor growth, and metastasis, while overexpression has opposite effects.
  • ELTD1 promotes epithelial to mesenchymal transition (EMT) by activating MAPK/ERK signaling through inhibition of CSK.
  • High ELTD1 expression is associated with poorer prognosis in GC patients, and the combination of ELTD1 and CSK improves predictive performance.

Conclusions:

  • ELTD1 functions as an oncogene in GC by promoting metastasis via the MAPK/ERK signaling pathway through CSK inhibition.
  • ELTD1 represents a potential prognostic predictor and therapeutic target for gastric cancer.
  • Targeting ELTD1 may offer a novel strategy for managing GC metastasis.
Keywords:
C-terminal Src kinaseEMTepidermal growth factorlatrophilin and seven-transmembrane domain-containing 1prognosis

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