E2F2 inhibition induces autophagy via the PI3K/Akt/mTOR pathway in gastric cancer

Hui Li1, Shufen Zhao1, Liwei Shen2

  • 1Department of Oncology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, China.

Aging
|June 6, 2021
PubMed
Abstract

Insights

High E2F2 expression in gastric cancer (GC) correlates with poor prognosis and promotes tumor cell invasion. This study reveals E2F2

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Cell Biology

Background:

  • E2F2, a transcription factor, has poorly understood roles in cancer.
  • The specific function of E2F2 in gastric cancer (GC) is unclear.

Purpose of the Study:

  • To investigate the expression and function of E2F2 in gastric cancer.
  • To explore the relationship between E2F2 and cancer progression, signaling pathways, and tumor immunity.

Main Methods:

  • Analyzed E2F2 expression in GC using public datasets (TIMER, Oncomine, GEPIA, UALCAN) and patient samples.
  • Utilized qRT-PCR, Western blotting, and immunohistochemistry for expression analysis.
  • Assessed the impact of E2F2 on PI3K/Akt/mTOR signaling, autophagy, and cell migration/invasion via wound healing, Transwell, and electron microscopy assays.

Main Results:

  • E2F2 was significantly upregulated in GC tissues and cells.
  • High E2F2 expression correlated with unfavorable overall survival (OS) and immune markers.
  • E2F2 overexpression enhanced GC cell migration and invasion by inhibiting PI3K/Akt/mTOR-mediated autophagy.

Conclusions:

  • Elevated E2F2 expression is linked to invasive tumor characteristics and poor prognosis in GC.
  • E2F2 plays a role in regulating tumor immunity.
  • Discovered a novel function of E2F2 in controlling PI3K/Akt/mTOR-mediated autophagy, impacting cell migration and invasion.

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