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  3. Research Domains
  5. Biomedical And Clinical Sciences
  7. Oncology And Carcinogenesis
  9. Predictive And Prognostic Markers
  11. Eif3b Affects The Invasion And Metastasis Of Hepatocellular Carcinoma Cells Via The Tgfbi/mapk/erk Pathway.
  1. Home
  3. Research Domains
  5. Biomedical And Clinical Sciences
  7. Oncology And Carcinogenesis
  9. Predictive And Prognostic Markers
  11. Eif3b Affects The Invasion And Metastasis Of Hepatocellular Carcinoma Cells Via The Tgfbi/mapk/erk Pathway.

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EIF3B affects the invasion and metastasis of hepatocellular carcinoma cells via the TGFBI/MAPK/ERK pathway.

Ling Wang1, Chuanzhong Huang1, Wansong Lin1

  • 1Laboratory of Immuno-Oncology, Clinical Oncology School of Fujian Medical University, Fujian Cancer Hospital, Fuzhou 350014,China; Fujian Key Laboratory of Translational Cancer Medicine, Fuzhou 350014, China.

Annals of Hepatology
|September 14, 2024

View abstract on PubMed

Summary
This summary is machine-generated.

Eukaryotic initiation factor 3B (EIF3B) promotes hepatocellular carcinoma (HCC) invasion and metastasis by activating the TGFBI/MAPK/ERK pathway. Targeting EIF3B may offer a new therapeutic strategy for HCC treatment.

Keywords:
EIF3BHepatocellular carcinomaInvasionMetastasis

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Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Hepatocellular carcinoma (HCC) is a major global health concern with limited treatment options.
  • Understanding the molecular mechanisms driving HCC progression is crucial for developing effective therapies.

Purpose of the Study:

  • To investigate the role of eukaryotic initiation factor 3B (EIF3B) in HCC invasion and migration.
  • To elucidate the underlying molecular mechanisms, including signaling pathways involved.

Main Methods:

  • Analysis of EIF3B expression in HCC using TCGA and GEPIA datasets.
  • In vitro assays (scratch, Transwell) to assess HCC cell invasion and metastasis.
  • RNA-seq to identify dysregulated pathways and western blotting to validate signaling alterations.
TGFBI-MAPK-ERK

Main Results:

  • Elevated EIF3B expression in HCC correlates with advanced tumor grade and poor prognosis.
  • EIF3B knockdown inhibited HCC cell invasion, metastasis, and epithelial-mesenchymal transition (EMT).
  • EIF3B activates the TGFBI/MAPK/ERK signaling pathway, increasing pMEK and pERK levels.

Conclusions:

  • EIF3B acts as an oncogene in HCC, promoting cell invasion, metastasis, and EMT.
  • EIF3B stimulates the TGFBI/MAPK/ERK signaling pathway.
  • EIF3B represents a potential therapeutic target for HCC treatment.