E2F3/CDCA2 reduces radiosensitivity in gastric adenocarcinoma by activating PI3K/AKT pathway

Jun Gao1, Huaqiao Wang1, Xiujuan Qiu2

  • 1Department of General Surgery, Xiangyang No.1 People's Hospital, Hubei University of Medicine, Xiangyang, China.

PubMed
Abstract

Insights

The E2F3/CDCA2 axis promotes gastric adenocarcinoma progression and reduces radiosensitivity by activating the PI3K/AKT pathway. This axis represents a potential new therapeutic target for this increasing global cancer.

Area of Science:

  • Oncology
  • Molecular Biology

Background:

  • Gastric adenocarcinoma is a leading cause of cancer deaths with rising incidence.
  • CDCA2, a nuclear protein, is implicated in promoting tumor growth.

Purpose of the Study:

  • To investigate the role of CDCA2 in gastric adenocarcinoma progression and radiosensitivity.
  • To elucidate the underlying molecular mechanisms involving CDCA2.

Main Methods:

  • Bioinformatic analysis to identify differentially expressed genes and upstream regulators.
  • Quantitative real-time PCR (qRT-PCR) and molecular experiments to validate regulatory relationships.
  • Cell viability (CCK-8), proliferation, and radiosensitivity assays (colony formation), and Western blot analysis of the PI3K/AKT pathway.

Main Results:

  • CDCA2 was significantly upregulated in gastric adenocarcinoma, promoting proliferation and decreasing radiosensitivity.
  • The PI3K/AKT pathway inhibitor reversed the effects of CDCA2 on proliferation and radiosensitivity.
  • E2F3 was identified as an upstream transcription factor that activates CDCA2, driving proliferation and reducing radiosensitivity via the PI3K/AKT pathway.

Conclusions:

  • The E2F3/CDCA2 axis promotes gastric adenocarcinoma cell proliferation and reduces radiosensitivity.
  • This axis operates through the activation of the PI3K/AKT pathway.
  • The E2F3/CDCA2 axis presents a novel therapeutic target for gastric adenocarcinoma.

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