Silence of ATAD2 inhibits proliferation of colorectal carcinoma via the Rb-E2F1 signaling

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Development and Maintenance of a Preclinical Patient Derived Tumor Xenograft Model for the Investigation of Novel Anti-Cancer Therapies
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J-H Wang1, T-T Yu, Y Li

  • 1Department of Gastroenterology, The First People's Hospital of Yancheng, Yancheng, China. xuping_1988@163.com.

European Review for Medical and Pharmacological Sciences
|June 24, 2020
PubMed
Abstract

Insights

ATPase family, AAA domain containing 2 (ATAD2) is upregulated in colorectal cancer (CRC) and linked to poor prognosis. Reducing ATAD2 inhibits CRC cell proliferation and promotes apoptosis.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Colorectal carcinoma (CRC) is a significant global health concern.
  • Understanding the molecular mechanisms driving CRC proliferation and apoptosis is crucial for developing effective therapies.

Purpose of the Study:

  • To investigate the role of ATPase family, AAA domain containing 2 (ATAD2) in regulating the proliferative and apoptotic capacities of colorectal carcinoma.
  • To determine the prognostic value of ATAD2 expression in CRC patients.

Main Methods:

  • ATAD2 expression levels were quantified in CRC specimens and cell lines using qRT-PCR.
  • Kaplan-Meier analysis assessed overall survival in relation to ATAD2 levels.
  • Functional experiments, including ATAD2 knockdown, were performed to evaluate its effects on cell viability, clonality, cell cycle, and apoptosis.
  • Western blot analysis detected key proteins involved in cell cycle regulation and apoptosis.

Main Results:

  • ATAD2 was found to be upregulated in CRC tissues and correlated with advanced tumor size, TNM staging, and histological classification.
  • High ATAD2 expression was associated with a poor prognosis in CRC patients.
  • ATAD2 knockdown significantly reduced CRC cell viability and clonality, induced G1 phase cell cycle arrest, and promoted apoptosis.
  • Knockdown of ATAD2 led to downregulation of Cyclin D1, ppRb, E2F1, and Cyclin E, and upregulation of cleaved Caspase 3.

Conclusions:

  • ATAD2 is frequently upregulated in colorectal cancer and serves as an independent prognostic factor for poor survival.
  • ATAD2 promotes CRC proliferation by regulating cell cycle progression and inhibiting apoptosis.
  • Targeting ATAD2 may represent a potential therapeutic strategy for colorectal cancer by inhibiting proliferation and inducing apoptosis through the Rb-E2F1 signaling pathway.

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