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IMP4 Silencing Inhibits the Malignancy of Lung Adenocarcinoma via ERK Pathway

Ruzhen Li1, Zhaohui Han1, Wei Ma1

  • 1Department of Thoracic Surgery, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, China.

Journal of Oncology
|November 1, 2022
PubMed

Insights

IMP U3 small nucleolar ribonucleoprotein 4 (IMP4) promotes lung adenocarcinoma (LUAD) growth and glycolysis by activating the ERK pathway. Silencing IMP4 inhibits LUAD progression and tumor growth.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Lung adenocarcinoma (LUAD) is a major cause of cancer-related mortality.
  • Understanding the molecular drivers of LUAD progression is crucial for developing effective therapies.

Purpose of the Study:

  • To investigate the role and molecular mechanisms of IMP U3 small nucleolar ribonucleoprotein 4 (IMP4) in LUAD.
  • To determine if IMP4 influences LUAD cell behavior and tumor growth via the extracellular signal-regulated kinase (ERK) pathway.

Main Methods:

  • Assessed LUAD cell proliferation, migration, invasion, apoptosis, and cell cycle using various assays.
  • Quantified IMP4 mRNA and protein expression via qRT-PCR, Western blotting, and immunohistochemistry.
  • Evaluated IMP4's role in tumor progression using a mouse xenograft model and measured glycolysis indicators.

Main Results:

  • IMP4 expression was significantly upregulated in human LUAD tissues and cells.
  • IMP4 silencing suppressed LUAD cell proliferation, migration, invasion, and glycolysis, while promoting apoptosis and cell cycle arrest.
  • IMP4 silencing inactivated the ERK pathway, and its effects were reversed by an ERK inhibitor; in vivo studies confirmed tumor growth and glycolysis inhibition.

Conclusions:

  • IMP4 acts as an oncogene in LUAD by promoting cell proliferation, migration, invasion, and glycolysis.
  • IMP4 exerts its oncogenic functions, at least in part, by activating the ERK signaling pathway.
  • Targeting IMP4 or the ERK pathway may represent a potential therapeutic strategy for LUAD.

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