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Eukaryotic initiation factor-2, gamma subunit, suppresses proliferation and regulates the cell cycle via the MAPK/ERK

Jielun Lu1,2, Shuyi Chen3,2, Huo Tan3

  • 1Department of Pediatrics, The First Affiliated Hospital of Guangzhou Medical University, 151 Yanjiang West Road, Yuexiu, Guangzhou, 510000, Guangdong, People's Republic of China.

Journal of Cancer Research and Clinical Oncology
|July 7, 2021
PubMed
Abstract

Insights

Eukaryotic translation initiation factor-2 subunit 3 (EIF2S3) is downregulated in acute myeloid leukemia (AML). Overexpression of EIF2S3 inhibits AML cell proliferation and tumorigenicity by affecting the MAPK/ERK signaling pathway.

Area of Science:

  • Molecular Biology
  • Oncology

Background:

  • Eukaryotic translation initiation factor-2 subunit 3 (EIF2S3) expression is reduced in non-small cell lung and colorectal cancers.
  • The role of EIF2S3 in leukemia remains largely unexplored.

Purpose of the Study:

  • To investigate the function of EIF2S3 in acute myeloid leukemia (AML).
  • To elucidate the underlying molecular mechanisms of EIF2S3 in AML.

Main Methods:

  • Quantitative PCR to assess EIF2S3 expression and correlate with AML patient prognosis.
  • Establishment of inducible HEL-EIF2S3 and HL-60-EIF2S3 cell lines.
  • Cell proliferation, cell cycle, and tumorigenicity assays (in vitro and in vivo).
  • Next-generation sequencing and Western blot analysis to identify molecular pathways involved.

Main Results:

  • EIF2S3 expression was significantly lower in AML patients compared to those in complete remission (CR).
  • Overexpression of EIF2S3 suppressed AML cell proliferation, induced cell cycle arrest at the G0/1 to S phase transition, and inhibited tumor formation.
  • Next-generation sequencing identified 479 differentially expressed genes, with several linked to the MAPK/ERK signaling pathway.
  • MAPK/ERK signaling pathway activity, indicated by ERK phosphorylation, was decreased upon EIF2S3 overexpression.

Conclusions:

  • EIF2S3 overexpression exerts tumor-suppressive effects in AML.
  • The observed inhibition of proliferation and tumorigenicity is mediated through the MAPK/ERK signaling pathway.
  • EIF2S3 represents a potential therapeutic target in AML.
Keywords:
Acute myeloid leukemiaCellular proliferationEIF2S3MAPK/ERK signaling pathwayPrognosisThe cell cycle

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